Subset of helper-inducer T-lymphocytes which synthesize and secrete the interleukins IL-4, IL-5, IL-6, and IL-10. These cytokines influence B-cell development and antibody production as well as augmenting humoral responses.
Subset of helper-inducer T-lymphocytes which synthesize and secrete interleukin-2, gamma-interferon, and interleukin-12. Due to their ability to kill antigen-presenting cells and their lymphokine-mediated effector activity, Th1 cells are associated with vigorous delayed-type hypersensitivity reactions.
Subset of helper-effector T-lymphocytes which synthesize and secrete IL-17, IL-17F, and IL-22. These cytokines are involved in host defenses and tissue inflammation in autoimmune diseases.
Homeostatic control of the immune system by secretion of different cytokines by the Th1 and Th2 cells. The concentration dependent binding of the various cytokines to specific receptors determines the balance (or imbalance leading to disease).
A soluble factor produced by activated T-LYMPHOCYTES that induces the expression of MHC CLASS II GENES and FC RECEPTORS on B-LYMPHOCYTES and causes their proliferation and differentiation. It also acts on T-lymphocytes, MAST CELLS, and several other hematopoietic lineage cells.
A proinflammatory cytokine produced primarily by T-LYMPHOCYTES or their precursors. Several subtypes of interleukin-17 have been identified, each of which is a product of a unique gene.
Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.
Subpopulation of CD4+ lymphocytes that cooperate with other lymphocytes (either T or B) to initiate a variety of immune functions. For example, helper-inducer T-cells cooperate with B-cells to produce antibodies to thymus-dependent antigens and with other subpopulations of T-cells to initiate a variety of cell-mediated immune functions.
Time period from 1801 through 1900 of the common era.
The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES.
Time period from 1601 through 1700 of the common era.
Inbred BALB/c mice are a strain of laboratory mice that have been selectively bred to be genetically identical to each other, making them useful for scientific research and experiments due to their consistent genetic background and predictable responses to various stimuli or treatments.
Time period from 1901 through 2000 of the common era.
Time period from 1701 through 1800 of the common era.
Inbred C57BL mice are a strain of laboratory mice that have been produced by many generations of brother-sister matings, resulting in a high degree of genetic uniformity and homozygosity, making them widely used for biomedical research, including studies on genetics, immunology, cancer, and neuroscience.
Time period from 1401 through 1500 of the common era.
A critical subpopulation of T-lymphocytes involved in the induction of most immunological functions. The HIV virus has selective tropism for the T4 cell which expresses the CD4 phenotypic marker, a receptor for HIV. In fact, the key element in the profound immunosuppression seen in HIV infection is the depletion of this subset of T-lymphocytes.
Time period from 1501 through 1600 of the common era.
A GATA transcription factor that is found predominately in LYMPHOID CELL precursors and has been implicated in the CELL DIFFERENTIATION of HELPER T-CELLS. Haploinsufficiency of GATA3 is associated with HYPOPARATHYROIDISM; SENSORINEURAL HEARING LOSS; and renal anomalies syndrome.
Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION.
A heterodimeric cytokine that plays a role in innate and adaptive immune responses. Interleukin-12 is a 70 kDa protein that is composed of covalently linked 40 kDa and 35 kDa subunits. It is produced by DENDRITIC CELLS; MACROPHAGES and a variety of other immune cells and plays a role in the stimulation of INTERFERON-GAMMA production by T-LYMPHOCYTES and NATURAL KILLER CELLS.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
A classification of T-lymphocytes, especially into helper/inducer, suppressor/effector, and cytotoxic subsets, based on structurally or functionally different populations of cells.
An albumin obtained from the white of eggs. It is a member of the serpin superfamily.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
An enzyme that catalyzes the conversion of L-tyrosine, tetrahydrobiopterin, and oxygen to 3,4-dihydroxy-L-phenylalanine, dihydrobiopterin, and water. EC 1.14.16.2.
Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli.
A cytokine produced by a variety of cell types, including T-LYMPHOCYTES; MONOCYTES; DENDRITIC CELLS; and EPITHELIAL CELLS that exerts a variety of effects on immunoregulation and INFLAMMATION. Interleukin-10 combines with itself to form a homodimeric molecule that is the biologically active form of the protein.
An orphan nuclear receptor found in the THYMUS where it plays a role in regulating the development and maturation of thymocytes. An isoform of this protein, referred to as RORgammaT, is produced by an alternatively transcribed mRNA.
Specialized cells of the hematopoietic system that have branch-like extensions. They are found throughout the lymphatic system, and in non-lymphoid tissues such as SKIN and the epithelia of the intestinal, respiratory, and reproductive tracts. They trap and process ANTIGENS, and present them to T-CELLS, thereby stimulating CELL-MEDIATED IMMUNITY. They are different from the non-hematopoietic FOLLICULAR DENDRITIC CELLS, which have a similar morphology and immune system function, but with respect to humoral immunity (ANTIBODY PRODUCTION).
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
A cytokine synthesized by T-LYMPHOCYTES that produces proliferation, immunoglobulin isotype switching, and immunoglobulin production by immature B-LYMPHOCYTES. It appears to play a role in regulating inflammatory and immune responses.
A cytokine that promotes differentiation and activation of EOSINOPHILS. It also triggers activated B-LYMPHOCYTES to differentiate into IMMUNOGLOBULIN-secreting cells.
CD4-positive T cells that inhibit immunopathology or autoimmune disease in vivo. They inhibit the immune response by influencing the activity of other cell types. Regulatory T-cells include naturally occurring CD4+CD25+ cells, IL-10 secreting Tr1 cells, and Th3 cells.
A heterodimeric cytokine that plays a role in innate and adaptive immune responses. Interleukin-23 is comprised of a unique 19 kDa subunit and 40 kDa subunit that is shared with INTERLEUKIN-12. It is produced by DENDRITIC CELLS; MACROPHAGES and a variety of other immune cells
Proteins containing a region of conserved sequence, about 200 amino acids long, which encodes a particular sequence specific DNA binding domain (the T-box domain). These proteins are transcription factors that control developmental pathways. The prototype of this family is the mouse Brachyury (or T) gene product.
Substances that augment, stimulate, activate, potentiate, or modulate the immune response at either the cellular or humoral level. The classical agents (Freund's adjuvant, BCG, Corynebacterium parvum, et al.) contain bacterial antigens. Some are endogenous (e.g., histamine, interferon, transfer factor, tuftsin, interleukin-1). Their mode of action is either non-specific, resulting in increased immune responsiveness to a wide variety of antigens, or antigen-specific, i.e., affecting a restricted type of immune response to a narrow group of antigens. The therapeutic efficacy of many biological response modifiers is related to their antigen-specific immunoadjuvanticity.
An encapsulated lymphatic organ through which venous blood filters.
A signal transducer and activator of transcription that mediates cellular responses to INTERLEUKIN-4. Stat6 has been shown to partner with NF-KAPPA B and CCAAT-ENHANCER-BINDING PROTEINS to regulate GENETIC TRANSCRIPTION of interleukin-4 responsive GENES.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
Form of passive immunization where previously sensitized immunologic agents (cells or serum) are transferred to non-immune recipients. When transfer of cells is used as a therapy for the treatment of neoplasms, it is called adoptive immunotherapy (IMMUNOTHERAPY, ADOPTIVE).
An immunoglobulin associated with MAST CELLS. Overexpression has been associated with allergic hypersensitivity (HYPERSENSITIVITY, IMMEDIATE).
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
A signal transducer and activator of transcription that mediates cellular responses to INTERLEUKIN-12 in T-LYMPHOCYTES. Stat4 is an important signaling molecule for differentiation in TH1 CELLS.
An experimental animal model for central nervous system demyelinating disease. Inoculation with a white matter emulsion combined with FREUND'S ADJUVANT, myelin basic protein, or purified central myelin triggers a T cell-mediated immune response directed towards central myelin. The pathologic features are similar to MULTIPLE SCLEROSIS, including perivascular and periventricular foci of inflammation and demyelination. Subpial demyelination underlying meningeal infiltrations also occurs, which is also a feature of ENCEPHALOMYELITIS, ACUTE DISSEMINATED. Passive immunization with T-cells from an afflicted animal to a normal animal also induces this condition. (From Immunol Res 1998;17(1-2):217-27; Raine CS, Textbook of Neuropathology, 2nd ed, p604-5)
Antigen-type substances that produce immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE).

Prevention of collagen-induced arthritis by gene delivery of soluble p75 tumour necrosis factor receptor. (1/5809)

Collagen type II-induced arthritis (CIA) in DBA/1 mice can be passively transferred to SCID mice with spleen B- and T-lymphocytes. In the present study, we show that infection ex vivo of splenocytes from arthritic DBA/1 mice with a retroviral vector, containing cDNA for the soluble form of human p75 receptor of tumour necrosis factor (TNF-R) before transfer, prevents the development of arthritis, bone erosion and joint inflammation in the SCID recipients. Assessment of IgG subclass levels and studies of synovial histology suggest that down-regulating the effector functions of T helper-type 1 (Th1) cells may, at least in part, explain the inhibition of arthritis in the SCID recipients. In contrast, the transfer of splenocytes infected with mouse TNF-alpha gene construct resulted in exacerbated arthritis and enhancement of IgG2a antibody levels. Intriguingly, infection of splenocytes from arthritic DBA/1 mice with a construct for mouse IL-10 had no modulating effect on the transfer of arthritis. The data suggest that manipulation of the immune system with cytokines, or cytokine inhibitors using gene transfer protocols can be an effective approach to ameliorate arthritis.  (+info)

Enhanced Th1 activity and development of chronic enterocolitis in mice devoid of Stat3 in macrophages and neutrophils. (2/5809)

We have generated mice with a cell type-specific disruption of the Stat3 gene in macrophages and neutrophils. The mutant mice are highly susceptible to endotoxin shock with increased production of inflammatory cytokines such as TNF alpha, IL-1, IFN gamma, and IL-6. Endotoxin-induced production of inflammatory cytokines is augmented because the suppressive effects of IL-10 on inflammatory cytokine production from macrophages and neutrophils are completely abolished. The mice show a polarized immune response toward the Th1 type and develop chronic enterocolitis with age. Taken together, Stat3 plays a critical role in deactivation of macrophages and neutrophils mainly exerted by IL-10.  (+info)

Interleukin-18 binding protein: a novel modulator of the Th1 cytokine response. (3/5809)

An interleukin-18 binding protein (IL-18BP) was purified from urine by chromatography on IL-18 beads, sequenced, cloned, and expressed in COS7 cells. IL-18BP abolished IL-18 induction of interferon-gamma (IFNgamma), IL-8, and activation of NF-kappaB in vitro. Administration of IL-18BP to mice abrogated circulating IFNgamma following LPS. Thus, IL-18BP functions as an inhibitor of the early Th1 cytokine response. IL-18BP is constitutively expressed in the spleen, belongs to the immunoglobulin superfamily, and has limited homology to the IL-1 type II receptor. Its gene was localized on human chromosome 11q13, and no exon coding for a transmembrane domain was found in an 8.3 kb genomic sequence. Several Poxviruses encode putative proteins highly homologous to IL-18BP, suggesting that viral products may attenuate IL-18 and interfere with the cytotoxic T cell response.  (+info)

Reciprocal control of T helper cell and dendritic cell differentiation. (4/5809)

It is not known whether subsets of dendritic cells provide different cytokine microenvironments that determine the differentiation of either type-1 T helper (TH1) or TH2 cells. Human monocyte (pDC1)-derived dendritic cells (DC1) were found to induce TH1 differentiation, whereas dendritic cells (DC2) derived from CD4+CD3-CD11c- plasmacytoid cells (pDC2) induced TH2 differentiation by use of a mechanism unaffected by interleukin-4 (IL-4) or IL-12. The TH2 cytokine IL-4 enhanced DC1 maturation and killed pDC2, an effect potentiated by IL-10 but blocked by CD40 ligand and interferon-gamma. Thus, a negative feedback loop from the mature T helper cells may selectively inhibit prolonged TH1 or TH2 responses by regulating survival of the appropriate dendritic cell subset.  (+info)

Enhanced Th1 and dampened Th2 responses synergize to inhibit acute granulomatous and fibrotic responses in murine schistosomiasis mansoni. (5/5809)

In murine schistosomiasis mansoni, CD4(+) Th1 and Th2 cells participate in the ovum-induced granulomatous inflammation. Previous studies showed that the interleukin-12 (IL-12)-induced Th1 response strongly suppressed the Th2-cell-mediated pulmonary granuloma development in naive or primed mice. However, liver granulomas were only moderately suppressed in egg-vaccinated, recombinant IL-12 (rIL-12)-treated infected mice. The present study shows that repeated rIL-12 injections given during early granuloma development at 5 to 7 weeks after infection prolonged the Th1 phase and resulted in gamma interferon-mediated suppression of liver granulomas. The timing is crucial: if given at 6 to 8 weeks, during the Th2-dominated phase of florid granuloma growth, the treatment is ineffective. Daily injections of rIL-12 given between 5 and 7.5 weeks during the period of granuloma growth achieved a somewhat-stronger diminution in granuloma growth with less deposition of collagen but caused 60% mortality and liver pathology. In contrast, combined treatment with rIL-12 and anti-IL-4-anti-IL-10 monoclonal antibody (MAb) injections given during the Th2 phase strongly inhibited liver granuloma growth without mortality. The diminished inflammatory response was accompanied by less deposition of collagen in the liver. Moreover, neutralization of endogenous IL-12 by anti-IL-12 MAbs effectively decreased the early Th1 phase (between 5 and 6 weeks after infection) but not the developing Th2 phase (5 to 7 weeks) of granuloma development. These studies indicate that the granulomatous response in infected mice can be manipulated by utilizing the Th1-Th2-subset antagonism with potential salutary results in the amelioration of fibrous pathology.  (+info)

Interleukin-10 inhibits expression of both interferon alpha- and interferon gamma- induced genes by suppressing tyrosine phosphorylation of STAT1. (6/5809)

Interleukin-10 (IL-10) helps maintain polarized T-helper cells in a T-helper lymphocyte 2 (Th2) phenotype. Part of this process involves the prevention of the development of Th1 cells, which are a primary source of interferon gamma (IFNgamma), a potent activator of monocytes and an inhibitor of Th2 proliferation. Because monocytes and macrophages are important mediators of Th1-type responses, such as delayed-type hypersensitivity, we sought to determine if IL-10 could directly mediate inhibition of IFNgamma- and IFNalpha-induced gene expression in these cells. Highly purified monocytes were incubated with IL-10 for 60 to 90 minutes before the addition of IFNgamma or IFNalpha. IL-10 preincubation resulted in the inhibition of gene expression for several IFN-induced genes, such as IP-10, ISG54, and intercellular adhesion molecule-1. The reduction in gene expression resulted from the ability of IL-10 to suppress IFN-induced assembly of signal transducer and activator of transcription (STAT) factors to specific promoter motifs on IFNalpha- and IFNgamma-inducible genes. This was accomplished by preventing the IFN-induced tyrosine phosphorylation of STAT1, a component of both IFNalpha- and IFNgamma-induced DNA binding complexes. Therefore, IL-10 can directly inhibit STAT-dependent early response gene expression induced by both IFNalpha and IFNgamma in monocytes by suppressing the tyrosine phosphorylation of STAT1. This may occur through the ability of IL-10 to induce expression of the gene, suppressor of cytokine signaling 3 (SOCS3).  (+info)

Interleukin-12 induces expression of interferon regulatory factor-1 via signal transducer and activator of transcription-4 in human T helper type 1 cells. (7/5809)

IRF-1-deficient mice show a striking defect in the development of T helper 1 (Th1) cells. In the present report, we investigate the expression of IRF-1 during differentiation of human T helper cells. No significant differences of IRF-1 mRNA expression were found in established Th1 and Th2 cells; however, interleukin 12 (IL-12) induced a strong up-regulation of IRF-1 transcripts in Th1 but not in Th2 cells. We demonstrate that IL-12-induced up-regulation of IRF-1 is mediated by signal transducer and activator of transcription-4, which binds to the interferon (IFN)-gamma-activated sequence present in the promoter of the IRF-1 gene. Strong IL-12-dependent activation of a reporter gene construct containing the IRF-1 IFN-gamma-activated sequence element provides further evidence for the key role of signal transducer and activator of transcription-4 in the IL-12-induced up-regulation of IRF-1 transcripts in T cells. IRF-1 expression was strongly induced after stimulation of naive CD4(+) T cells via the T cell receptor, irrespective of the cytokines present at priming, indicating that this transcription factor does not play a major role in initiating a Th1-specific transcriptional cascade in differentiating helper T cells. However, our finding that IRF-1 is a target gene of IL-12 suggests that some of the IL-12-induced effector functions of Th1 cells may be mediated by IRF-1.  (+info)

Cytokine network and resident renal cells in glomerular diseases. (8/5809)

This review has highlighted the cytokine network which is involved in renal damage from an initial, even transient, stage to extensive glomerular and tubulointerstitial sclerosis. Studies of a variety of different proliferative glomerulonephritides have documented the prominent role of macrophages in infiltrating mesangium, subendothelial area and crescentic formation. Thus, they stimulate crescent glomerular cells to produce other cytokines and growth factors. The identification of other mediators, released by the monocytes in the interstitium, exemplifies the important role of these cells in progressive interstitial scarring through the release of fibrogenic cytokines. In addition, renal tubular cells have been found to produce a vast array of cytokines and growth factors which participate in the generation of renal interstitial scarring.  (+info)

Th2 cells, or T helper 2 cells, are a type of CD4+ T cell that plays a key role in the immune response to parasites and allergens. They produce cytokines such as IL-4, IL-5, IL-13 which promote the activation and proliferation of eosinophils, mast cells, and B cells, leading to the production of antibodies such as IgE. Th2 cells also play a role in the pathogenesis of allergic diseases such as asthma, atopic dermatitis, and allergic rhinitis.

It's important to note that an imbalance in Th1/Th2 response can lead to immune dysregulation and disease states. For example, an overactive Th2 response can lead to allergic reactions while an underactive Th2 response can lead to decreased ability to fight off parasitic infections.

It's also worth noting that there are other subsets of CD4+ T cells such as Th1, Th17, Treg and others, each with their own specific functions and cytokine production profiles.

Th1 cells, or Type 1 T helper cells, are a subset of CD4+ T cells that play a crucial role in the cell-mediated immune response. They are characterized by the production of specific cytokines, such as interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), and interleukin-2 (IL-2). Th1 cells are essential for protecting against intracellular pathogens, including viruses, bacteria, and parasites. They activate macrophages to destroy ingested microorganisms, stimulate the differentiation of B cells into plasma cells that produce antibodies, and recruit other immune cells to the site of infection. Dysregulation of Th1 cell responses has been implicated in various autoimmune diseases, such as multiple sclerosis, rheumatoid arthritis, and type 1 diabetes.

T helper 17 (Th17) cells are a subset of CD4+ T cells, which are a type of white blood cell that plays a crucial role in the immune response. Th17 cells are characterized by their production of certain cytokines, including interleukin-17 (IL-17), IL-21, and IL-22. They are involved in the inflammatory response and play a key role in protecting the body against extracellular bacteria and fungi. However, an overactive Th17 response has been implicated in several autoimmune diseases, such as multiple sclerosis, rheumatoid arthritis, and psoriasis. Therefore, understanding the regulation of Th17 cells is important for developing new therapies to treat these conditions.

Th1-Th2 balance refers to the regulation of the immune response by two subsets of T helper cells, Th1 and Th2. These cell types produce different cytokines that mediate distinct types of immune responses. A balanced Th1-Th2 response is critical for maintaining immune homeostasis and protecting the body against various pathogens.

Th1 cells primarily mediate cell-mediated immunity, which involves activating macrophages, natural killer (NK) cells, and cytotoxic T lymphocytes (CTLs) to eliminate intracellular pathogens such as viruses and bacteria. Th1 cells produce cytokines like interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), and interleukin-2 (IL-2).

Th2 cells, on the other hand, mediate humoral immunity, which involves activating B cells to produce antibodies against extracellular pathogens like parasites and toxins. Th2 cells produce cytokines like interleukin-4 (IL-4), interleukin-5 (IL-5), interleukin-10 (IL-10), and interleukin-13 (IL-13).

An imbalance in the Th1-Th2 response can lead to various immune-related disorders. For example, an overactive Th1 response can result in autoimmune diseases, while an overactive Th2 response can contribute to allergic and atopic conditions like asthma and eczema. Therefore, maintaining a balanced Th1-Th2 response is crucial for optimal immune function and overall health.

Interleukin-4 (IL-4) is a type of cytokine, which is a cell signaling molecule that mediates communication between cells in the immune system. Specifically, IL-4 is produced by activated T cells and mast cells, among other cells, and plays an important role in the differentiation and activation of immune cells called Th2 cells.

Th2 cells are involved in the immune response to parasites, as well as in allergic reactions. IL-4 also promotes the growth and survival of B cells, which produce antibodies, and helps to regulate the production of certain types of antibodies. In addition, IL-4 has anti-inflammatory effects and can help to downregulate the immune response in some contexts.

Defects in IL-4 signaling have been implicated in a number of diseases, including asthma, allergies, and certain types of cancer.

Interleukin-17 (IL-17) is a type of cytokine, which are proteins that play a crucial role in cell signaling and communication during the immune response. IL-17 is primarily produced by a subset of T helper cells called Th17 cells, although other cell types like neutrophils, mast cells, natural killer cells, and innate lymphoid cells can also produce it.

IL-17 has several functions in the immune system, including:

1. Promoting inflammation: IL-17 stimulates the production of various proinflammatory cytokines, chemokines, and enzymes from different cell types, leading to the recruitment of immune cells like neutrophils to the site of infection or injury.
2. Defending against extracellular pathogens: IL-17 plays a critical role in protecting the body against bacterial and fungal infections by enhancing the recruitment and activation of neutrophils, which can engulf and destroy these microorganisms.
3. Regulating tissue homeostasis: IL-17 helps maintain the balance between immune tolerance and immunity in various tissues by regulating the survival, proliferation, and differentiation of epithelial cells, fibroblasts, and other structural components.

However, dysregulated IL-17 production or signaling has been implicated in several inflammatory and autoimmune diseases, such as psoriasis, rheumatoid arthritis, multiple sclerosis, and inflammatory bowel disease. Therefore, targeting the IL-17 pathway with specific therapeutics has emerged as a promising strategy for treating these conditions.

Cytokines are a broad and diverse category of small signaling proteins that are secreted by various cells, including immune cells, in response to different stimuli. They play crucial roles in regulating the immune response, inflammation, hematopoiesis, and cellular communication.

Cytokines mediate their effects by binding to specific receptors on the surface of target cells, which triggers intracellular signaling pathways that ultimately result in changes in gene expression, cell behavior, and function. Some key functions of cytokines include:

1. Regulating the activation, differentiation, and proliferation of immune cells such as T cells, B cells, natural killer (NK) cells, and macrophages.
2. Coordinating the inflammatory response by recruiting immune cells to sites of infection or tissue damage and modulating their effector functions.
3. Regulating hematopoiesis, the process of blood cell formation in the bone marrow, by controlling the proliferation, differentiation, and survival of hematopoietic stem and progenitor cells.
4. Modulating the development and function of the nervous system, including neuroinflammation, neuroprotection, and neuroregeneration.

Cytokines can be classified into several categories based on their structure, function, or cellular origin. Some common types of cytokines include interleukins (ILs), interferons (IFNs), tumor necrosis factors (TNFs), chemokines, colony-stimulating factors (CSFs), and transforming growth factors (TGFs). Dysregulation of cytokine production and signaling has been implicated in various pathological conditions, such as autoimmune diseases, chronic inflammation, cancer, and neurodegenerative disorders.

T-lymphocytes, also known as T-cells, are a type of white blood cell that plays a key role in the immune response. They help to protect the body from infection and disease by identifying and attacking foreign substances such as viruses and bacteria.

Helper-inducer T-lymphocytes, also known as CD4+ T-cells or Th0 cells, are a specific subset of T-lymphocytes that help to coordinate the immune response. They do this by activating other immune cells, such as B-lymphocytes (which produce antibodies) and cytotoxic T-lymphocytes (which directly attack infected cells). Helper-inducer T-lymphocytes also release cytokines, which are signaling molecules that help to regulate the immune response.

Helper-inducer T-lymphocytes can differentiate into different subsets of T-cells, depending on the type of cytokines they are exposed to. For example, they can differentiate into Th1 cells, which produce cytokines that help to activate cytotoxic T-lymphocytes and macrophages; or Th2 cells, which produce cytokines that help to activate B-lymphocytes and eosinophils.

It is important to note that helper-inducer T-lymphocytes play a crucial role in the immune response, and dysfunction of these cells can lead to immunodeficiency or autoimmune disorders.

"History, 19th Century" is not a medical term or concept. It refers to the historical events, developments, and figures related to the 1800s in various fields, including politics, culture, science, and technology. However, if you are looking for medical advancements during the 19th century, here's a brief overview:

The 19th century was a period of significant progress in medicine, with numerous discoveries and innovations that shaped modern medical practices. Some notable developments include:

1. Edward Jenner's smallpox vaccine (1796): Although not strictly within the 19th century, Jenner's discovery laid the foundation for vaccination as a preventive measure against infectious diseases.
2. Germ theory of disease: The work of Louis Pasteur, Robert Koch, and others established that many diseases were caused by microorganisms, leading to the development of antiseptic practices and vaccines.
3. Anesthesia: In 1842, Crawford Long first used ether as an anesthetic during surgery, followed by the introduction of chloroform in 1847 by James Simpson.
4. Antisepsis and asepsis: Joseph Lister introduced antiseptic practices in surgery, significantly reducing postoperative infections. Later, the concept of asepsis (sterilization) was developed to prevent contamination during surgical procedures.
5. Microbiology: The development of techniques for culturing and staining bacteria allowed for better understanding and identification of pathogens.
6. Physiology: Claude Bernard's work on the regulation of internal body functions, or homeostasis, contributed significantly to our understanding of human physiology.
7. Neurology: Jean-Martin Charcot made significant contributions to the study of neurological disorders, including multiple sclerosis and Parkinson's disease.
8. Psychiatry: Sigmund Freud developed psychoanalysis, a new approach to understanding mental illnesses.
9. Public health: The 19th century saw the establishment of public health organizations and initiatives aimed at improving sanitation, water quality, and vaccination programs.
10. Medical education reforms: The Flexner Report in 1910 led to significant improvements in medical education standards and practices.

Interferon-gamma (IFN-γ) is a soluble cytokine that is primarily produced by the activation of natural killer (NK) cells and T lymphocytes, especially CD4+ Th1 cells and CD8+ cytotoxic T cells. It plays a crucial role in the regulation of the immune response against viral and intracellular bacterial infections, as well as tumor cells. IFN-γ has several functions, including activating macrophages to enhance their microbicidal activity, increasing the presentation of major histocompatibility complex (MHC) class I and II molecules on antigen-presenting cells, stimulating the proliferation and differentiation of T cells and NK cells, and inducing the production of other cytokines and chemokines. Additionally, IFN-γ has direct antiproliferative effects on certain types of tumor cells and can enhance the cytotoxic activity of immune cells against infected or malignant cells.

I believe there might be a bit of confusion in your question. A "history" in medical terms usually refers to the detailed account of a patient's symptoms, illnesses, and treatments received, which is used by healthcare professionals to understand their health status and provide appropriate care. It is not typically associated with a specific century like the 17th century.

If you are asking for information about the medical practices or significant developments in the field of medicine during the 17th century, I would be happy to provide some insight into that. The 17th century was a time of great advancement in medical knowledge and practice, with several key figures and events shaping the course of medical history.

Some notable developments in medicine during the 17th century include:

1. William Harvey's discovery of the circulation of blood (1628): English physician William Harvey published his groundbreaking work "De Motu Cordis" (On the Motion of the Heart and Blood), which described the circulatory system and the role of the heart in pumping blood throughout the body. This discovery fundamentally changed our understanding of human anatomy and physiology.
2. The development of the microscope (1600s): The invention of the microscope allowed scientists to observe structures that were previously invisible to the naked eye, such as cells, bacteria, and other microorganisms. This technology opened up new avenues of research in anatomy, physiology, and pathology, paving the way for modern medical science.
3. The establishment of the Royal Society (1660): The Royal Society, a prominent scientific organization in the UK, was founded during this century to promote scientific inquiry and share knowledge among its members. Many notable scientists and physicians, including Robert Hooke and Christopher Wren, were part of the society and contributed significantly to the advancement of medical science.
4. The Smallpox Vaccination (1796): Although this occurred near the end of the 18th century, the groundwork for Edward Jenner's smallpox vaccine was laid during the 17th century. Smallpox was a significant public health issue during this time, and Jenner's development of an effective vaccine marked a major milestone in the history of medicine and public health.
5. The work of Sylvius de le Boe (1614-1672): A Dutch physician and scientist, Sylvius de le Boe made significant contributions to our understanding of human anatomy and physiology. He was the first to describe the circulation of blood in the lungs and identified the role of the liver in metabolism.

These are just a few examples of the many advancements that took place during the 17th century, shaping the course of medical history and laying the foundation for modern medicine.

BALB/c is an inbred strain of laboratory mouse that is widely used in biomedical research. The strain was developed at the Institute of Cancer Research in London by Henry Baldwin and his colleagues in the 1920s, and it has since become one of the most commonly used inbred strains in the world.

BALB/c mice are characterized by their black coat color, which is determined by a recessive allele at the tyrosinase locus. They are also known for their docile and friendly temperament, making them easy to handle and work with in the laboratory.

One of the key features of BALB/c mice that makes them useful for research is their susceptibility to certain types of tumors and immune responses. For example, they are highly susceptible to developing mammary tumors, which can be induced by chemical carcinogens or viral infection. They also have a strong Th2-biased immune response, which makes them useful models for studying allergic diseases and asthma.

BALB/c mice are also commonly used in studies of genetics, neuroscience, behavior, and infectious diseases. Because they are an inbred strain, they have a uniform genetic background, which makes it easier to control for genetic factors in experiments. Additionally, because they have been bred in the laboratory for many generations, they are highly standardized and reproducible, making them ideal subjects for scientific research.

I'm sorry for any confusion, but "History, 20th Century" is a broad and complex topic that refers to the events, developments, and transformations that occurred throughout the world during the 1900s. It is not a medical term or concept. If you're interested in learning more about this historical period, I would recommend consulting a history textbook, reputable online resources, or speaking with a historian. They can provide detailed information about the political, social, economic, and cultural changes that took place during the 20th century.

I believe there might be a bit of confusion in your question. A "history" in medical terms usually refers to the detailed account of a patient's symptoms, illnesses, and treatments received, which is used by healthcare professionals to understand their health status and provide appropriate care. It is not typically associated with a specific century like the 18th century.

If you are asking for information about the medical practices or significant developments in the field of medicine during the 18th century, I would be happy to provide some insight into that! The 18th century was a time of great advancement and change in the medical field, with many notable discoveries and innovations. Some examples include:

* The development of smallpox vaccination by Edward Jenner in 1796
* The discovery of oxygen by Joseph Priestley in 1774
* The invention of the thermometer by Gabriel Fahrenheit in 1714
* The publication of "An Inquiry into the Causes and Effects of the Variolae Vaccinae" by Edward Jenner in 1798, which helped to establish the concept of vaccination
* The founding of the Royal Society of Medicine in London in 1773
* The development of new surgical techniques and instruments, such as the use of tourniquets and catgut sutures.

C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.

The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.

C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.

One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.

Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.

I believe there might be a bit of confusion in your question. A "medical definition" refers to the explanation of a medical term or concept. On the other hand, "15th century" is a historical time period and does not have a medical definition per se. However, I can provide you with some context regarding the medical advancements and practices during the 15th century.

The 15th century was marked by significant developments in medicine, particularly in Europe, as it transitioned from medieval to early modern medicine. Some key aspects of 15th-century medicine include:

1. Universities and medical education: Universities became more prominent centers for medical education, with institutions like the University of Bologna, Padua, Montpellier, and Salamanca playing crucial roles in shaping medical thought. Medical faculties taught subjects such as anatomy, physiology, pathology, surgery, and pharmacology based on ancient Greek and Roman texts, mainly Galen and Hippocrates.

2. Anatomical studies: The 15th century saw the beginning of a more accurate understanding of human anatomy. Italian anatomist and physician Mondino de Luzzi (c. 1270–1326) is known for his influential anatomy textbook, "Anathomia," which was widely used during this period. Later in the century, Andreas Vesalius (1514–1564), often regarded as the founder of modern human anatomy, began his groundbreaking work on detailed dissections and accurate representations of the human body.

3. Renaissance of medical illustrations: The 15th century marked a revival in medical illustrations, with artists like Leonardo da Vinci (1452–1519) creating highly accurate anatomical drawings based on dissections. These detailed images helped physicians better understand the human body and its functions.

4. Development of hospitals: Hospitals during this time became more organized and specialized, focusing on specific medical conditions or patient populations. For example, mental health institutions, known as "madhouses" or "asylums," were established to treat individuals with mental illnesses.

5. Plague and public health: The ongoing threat of the bubonic plague (Black Death) led to increased efforts in public health, including improved sanitation practices and the establishment of quarantine measures for infected individuals.

6. Humoral theory: Although challenged by some during this period, the ancient Greek humoral theory—which posited that the balance of four bodily fluids or "humors" (blood, phlegm, black bile, and yellow bile) determined a person's health—remained influential in medical practice.

7. Surgery: Barber-surgeons continued to perform various surgical procedures, including bloodletting, tooth extraction, and amputations. However, anesthesia was still not widely used, and pain management relied on opium or alcohol-based preparations.

8. Pharmacology: The use of herbal remedies and other natural substances to treat illnesses remained popular during the 15th century. Physicians like Nicholas Culpeper (1616–1654) compiled extensive lists of medicinal plants and their uses, contributing to the development of modern pharmacology.

9. Astrology and medicine: Despite growing skepticism among some scholars, astrological beliefs continued to influence medical practice in the 15th century. Physicians often consulted astrological charts when diagnosing and treating patients.

10. Medical education: Universities across Europe offered formal medical education, with students studying anatomy, physiology, pathology, and pharmacology. However, many practitioners still learned their trade through apprenticeships or self-study.

CD4-positive T-lymphocytes, also known as CD4+ T cells or helper T cells, are a type of white blood cell that plays a crucial role in the immune response. They express the CD4 receptor on their surface and help coordinate the immune system's response to infectious agents such as viruses and bacteria.

CD4+ T cells recognize and bind to specific antigens presented by antigen-presenting cells, such as dendritic cells or macrophages. Once activated, they can differentiate into various subsets of effector cells, including Th1, Th2, Th17, and Treg cells, each with distinct functions in the immune response.

CD4+ T cells are particularly important in the immune response to HIV (human immunodeficiency virus), which targets and destroys these cells, leading to a weakened immune system and increased susceptibility to opportunistic infections. The number of CD4+ T cells is often used as a marker of disease progression in HIV infection, with lower counts indicating more advanced disease.

I believe there might be a bit of confusion in your question. A "history" in medical terms usually refers to the detailed account of a patient's symptoms, illnesses, and treatments over time. It is a crucial part of the medical record and helps healthcare professionals understand the patient's health status and inform their care plans.

On the other hand, "16th century" refers to a specific period in history, spanning from 1501 to 1600 AD.

There isn't a direct medical definition for 'History, 16th Century.' However, if you are interested in learning about the medical advancements and practices during that time, I would be happy to provide some information. The 16th century was marked by significant developments in anatomy, surgery, and pharmacology, thanks to pioneers like Andreas Vesalius, Ambroise Paré, and William Shakespeare, who incorporated medical themes into his plays.

GATA3 transcription factor is a protein that plays a crucial role in the development and function of various types of cells, particularly in the immune system and the nervous system. It belongs to the family of GATA transcription factors, which are characterized by their ability to bind to specific DNA sequences through a zinc finger domain.

The GATA3 protein is encoded by the GATA3 gene, which is located on chromosome 10 in humans. This protein contains two zinc fingers that allow it to recognize and bind to the GATAA sequence in the DNA. Once bound, GATA3 can regulate the transcription of nearby genes, either activating or repressing their expression.

In the immune system, GATA3 is essential for the development of T cells, a type of white blood cell that plays a central role in the adaptive immune response. Specifically, GATA3 helps to promote the differentiation of naive T cells into Th2 cells, which produce cytokines that are involved in the defense against parasites and allergens.

In addition to its role in the immune system, GATA3 has also been implicated in the development and function of the nervous system. For example, it has been shown to play a role in the differentiation of neural crest cells, which give rise to various types of cells in the peripheral nervous system.

Mutations in the GATA3 gene have been associated with several human diseases, including HDR syndrome (hypoparathyroidism, deafness, and renal dysplasia) and certain types of cancer, such as breast cancer and bladder cancer.

Lymphocyte activation is the process by which B-cells and T-cells (types of lymphocytes) become activated to perform effector functions in an immune response. This process involves the recognition of specific antigens presented on the surface of antigen-presenting cells, such as dendritic cells or macrophages.

The activation of B-cells leads to their differentiation into plasma cells that produce antibodies, while the activation of T-cells results in the production of cytotoxic T-cells (CD8+ T-cells) that can directly kill infected cells or helper T-cells (CD4+ T-cells) that assist other immune cells.

Lymphocyte activation involves a series of intracellular signaling events, including the binding of co-stimulatory molecules and the release of cytokines, which ultimately result in the expression of genes involved in cell proliferation, differentiation, and effector functions. The activation process is tightly regulated to prevent excessive or inappropriate immune responses that can lead to autoimmunity or chronic inflammation.

Interleukin-12 (IL-12) is a naturally occurring protein that is primarily produced by activated macrophages and dendritic cells, which are types of immune cells. It plays a crucial role in the regulation of the immune response, particularly in the development of cell-mediated immunity.

IL-12 is composed of two subunits, p35 and p40, which combine to form a heterodimer. This cytokine stimulates the differentiation and activation of naive T cells into Th1 cells, which are important for fighting intracellular pathogens such as viruses and bacteria. IL-12 also enhances the cytotoxic activity of natural killer (NK) cells and CD8+ T cells, which can directly kill infected or malignant cells.

In addition to its role in the immune response, IL-12 has been implicated in the pathogenesis of several autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, and psoriasis. As a result, therapeutic strategies targeting IL-12 or its signaling pathways have been explored as potential treatments for these conditions.

Cell differentiation is the process by which a less specialized cell, or stem cell, becomes a more specialized cell type with specific functions and structures. This process involves changes in gene expression, which are regulated by various intracellular signaling pathways and transcription factors. Differentiation results in the development of distinct cell types that make up tissues and organs in multicellular organisms. It is a crucial aspect of embryonic development, tissue repair, and maintenance of homeostasis in the body.

A "knockout" mouse is a genetically engineered mouse in which one or more genes have been deleted or "knocked out" using molecular biology techniques. This allows researchers to study the function of specific genes and their role in various biological processes, as well as potential associations with human diseases. The mice are generated by introducing targeted DNA modifications into embryonic stem cells, which are then used to create a live animal. Knockout mice have been widely used in biomedical research to investigate gene function, disease mechanisms, and potential therapeutic targets.

T-lymphocyte subsets refer to distinct populations of T-cells, which are a type of white blood cell that plays a central role in cell-mediated immunity. The two main types of T-lymphocytes are CD4+ and CD8+ cells, which are defined by the presence or absence of specific proteins called cluster differentiation (CD) molecules on their surface.

CD4+ T-cells, also known as helper T-cells, play a crucial role in activating other immune cells, such as B-lymphocytes and macrophages, to mount an immune response against pathogens. They also produce cytokines that help regulate the immune response.

CD8+ T-cells, also known as cytotoxic T-cells, directly kill infected cells or tumor cells by releasing toxic substances such as perforins and granzymes.

The balance between these two subsets of T-cells is critical for maintaining immune homeostasis and mounting effective immune responses against pathogens while avoiding excessive inflammation and autoimmunity. Therefore, the measurement of T-lymphocyte subsets is essential in diagnosing and monitoring various immunological disorders, including HIV infection, cancer, and autoimmune diseases.

Ovalbumin is the major protein found in egg white, making up about 54-60% of its total protein content. It is a glycoprotein with a molecular weight of around 45 kDa and has both hydrophilic and hydrophobic regions. Ovalbumin is a single polypeptide chain consisting of 385 amino acids, including four disulfide bridges that contribute to its structure.

Ovalbumin is often used in research as a model antigen for studying immune responses and allergies. In its native form, ovalbumin is not allergenic; however, when it is denatured or degraded into smaller peptides through cooking or digestion, it can become an allergen for some individuals.

In addition to being a food allergen, ovalbumin has been used in various medical and research applications, such as vaccine development, immunological studies, and protein structure-function analysis.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

Tyrosine 3-Monooxygenase (also known as Tyrosinase or Tyrosine hydroxylase) is an enzyme that plays a crucial role in the synthesis of catecholamines, which are neurotransmitters and hormones in the body. This enzyme catalyzes the conversion of the amino acid L-tyrosine to 3,4-dihydroxyphenylalanine (L-DOPA) by adding a hydroxyl group to the 3rd carbon atom of the tyrosine molecule.

The reaction is as follows:

L-Tyrosine + O2 + pterin (co-factor) -> L-DOPA + pterin (oxidized) + H2O

This enzyme requires molecular oxygen and a co-factor such as tetrahydrobiopterin to carry out the reaction. Tyrosine 3-Monooxygenase is found in various tissues, including the brain and adrenal glands, where it helps regulate the production of catecholamines like dopamine, norepinephrine, and epinephrine. Dysregulation of this enzyme has been implicated in several neurological disorders, such as Parkinson's disease.

Interleukins (ILs) are a group of naturally occurring proteins that are important in the immune system. They are produced by various cells, including immune cells like lymphocytes and macrophages, and they help regulate the immune response by facilitating communication between different types of cells. Interleukins can have both pro-inflammatory and anti-inflammatory effects, depending on the specific interleukin and the context in which it is produced. They play a role in various biological processes, including the development of immune responses, inflammation, and hematopoiesis (the formation of blood cells).

There are many different interleukins that have been identified, and they are numbered according to the order in which they were discovered. For example, IL-1, IL-2, IL-3, etc. Each interleukin has a specific set of functions and targets certain types of cells. Dysregulation of interleukins has been implicated in various diseases, including autoimmune disorders, infections, and cancer.

Interleukin-10 (IL-10) is an anti-inflammatory cytokine that plays a crucial role in the modulation of immune responses. It is produced by various cell types, including T cells, macrophages, and dendritic cells. IL-10 inhibits the production of pro-inflammatory cytokines, such as TNF-α, IL-1, IL-6, IL-8, and IL-12, and downregulates the expression of costimulatory molecules on antigen-presenting cells. This results in the suppression of T cell activation and effector functions, which ultimately helps to limit tissue damage during inflammation and promote tissue repair. Dysregulation of IL-10 has been implicated in various pathological conditions, including chronic infections, autoimmune diseases, and cancer.

Nuclear Receptor Subfamily 1, Group F, Member 3 (NR1F3) is a gene that encodes for the retinoic acid-related orphan receptor alpha (RORα) protein. RORα is a type of nuclear receptor, which are transcription factors that regulate gene expression in response to various signals, including hormones and other molecules. RORα plays important roles in several biological processes, such as the regulation of circadian rhythm, immune function, and metabolism.

NR1F3/RORα has been identified as a critical regulator of the development and function of various immune cells, including T cells, B cells, and dendritic cells. It is also involved in the regulation of lipid metabolism and energy homeostasis, and its dysregulation has been implicated in several metabolic disorders, such as obesity, type 2 diabetes, and non-alcoholic fatty liver disease.

Furthermore, NR1F3/RORα has been shown to play a role in the development of certain cancers, including breast cancer, prostate cancer, and leukemia. Therefore, understanding the function and regulation of NR1F3/RORα is an active area of research with potential therapeutic implications for various diseases.

Dendritic cells (DCs) are a type of immune cell that play a critical role in the body's defense against infection and cancer. They are named for their dendrite-like projections, which they use to interact with and sample their environment. DCs are responsible for processing antigens (foreign substances that trigger an immune response) and presenting them to T cells, a type of white blood cell that plays a central role in the immune system's response to infection and cancer.

DCs can be found throughout the body, including in the skin, mucous membranes, and lymphoid organs. They are able to recognize and respond to a wide variety of antigens, including those from bacteria, viruses, fungi, and parasites. Once they have processed an antigen, DCs migrate to the lymph nodes, where they present the antigen to T cells. This interaction activates the T cells, which then go on to mount a targeted immune response against the invading pathogen or cancerous cells.

DCs are a diverse group of cells that can be divided into several subsets based on their surface markers and function. Some DCs, such as Langerhans cells and dermal DCs, are found in the skin and mucous membranes, where they serve as sentinels for invading pathogens. Other DCs, such as plasmacytoid DCs and conventional DCs, are found in the lymphoid organs, where they play a role in activating T cells and initiating an immune response.

Overall, dendritic cells are essential for the proper functioning of the immune system, and dysregulation of these cells has been implicated in a variety of diseases, including autoimmune disorders and cancer.

Transgenic mice are genetically modified rodents that have incorporated foreign DNA (exogenous DNA) into their own genome. This is typically done through the use of recombinant DNA technology, where a specific gene or genetic sequence of interest is isolated and then introduced into the mouse embryo. The resulting transgenic mice can then express the protein encoded by the foreign gene, allowing researchers to study its function in a living organism.

The process of creating transgenic mice usually involves microinjecting the exogenous DNA into the pronucleus of a fertilized egg, which is then implanted into a surrogate mother. The offspring that result from this procedure are screened for the presence of the foreign DNA, and those that carry the desired genetic modification are used to establish a transgenic mouse line.

Transgenic mice have been widely used in biomedical research to model human diseases, study gene function, and test new therapies. They provide a valuable tool for understanding complex biological processes and developing new treatments for a variety of medical conditions.

Interleukin-13 (IL-13) is a cytokine that plays a crucial role in the immune response, particularly in the development of allergic inflammation and hypersensitivity reactions. It is primarily produced by activated Th2 cells, mast cells, basophils, and eosinophils. IL-13 mediates its effects through binding to the IL-13 receptor complex, which consists of the IL-13Rα1 and IL-4Rα chains.

IL-13 has several functions in the body, including:

* Regulation of IgE production by B cells
* Induction of eosinophil differentiation and activation
* Inhibition of proinflammatory cytokine production by macrophages
* Promotion of mucus production and airway hyperresponsiveness in the lungs, contributing to the pathogenesis of asthma.

Dysregulation of IL-13 has been implicated in various diseases, such as allergic asthma, atopic dermatitis, and chronic rhinosinusitis. Therefore, targeting IL-13 with biologic therapies has emerged as a promising approach for the treatment of these conditions.

Interleukin-5 (IL-5) is a type of cytokine, which is a small signaling protein that mediates and regulates immunity, inflammation, and hematopoiesis. IL-5 is primarily produced by activated T cells, especially Th2 cells, as well as mast cells, eosinophils, and innate lymphoid cells (ILCs).

The primary function of IL-5 is to regulate the growth, differentiation, activation, and survival of eosinophils, a type of white blood cell that plays a crucial role in the immune response against parasitic infections. IL-5 also enhances the ability of eosinophils to migrate from the bone marrow into the bloodstream and then into tissues, where they can participate in immune responses.

In addition to its effects on eosinophils, IL-5 has been shown to have a role in the regulation of B cell function, including promoting the survival and differentiation of B cells into antibody-secreting plasma cells. Dysregulation of IL-5 production and activity has been implicated in several diseases, including asthma, allergies, and certain parasitic infections.

Regulatory T-lymphocytes (Tregs), also known as suppressor T cells, are a subpopulation of T-cells that play a critical role in maintaining immune tolerance and preventing autoimmune diseases. They function to suppress the activation and proliferation of other immune cells, thereby regulating the immune response and preventing it from attacking the body's own tissues.

Tregs constitutively express the surface markers CD4 and CD25, as well as the transcription factor Foxp3, which is essential for their development and function. They can be further divided into subsets based on their expression of other markers, such as CD127 and CD45RA.

Tregs are critical for maintaining self-tolerance by suppressing the activation of self-reactive T cells that have escaped negative selection in the thymus. They also play a role in regulating immune responses to foreign antigens, such as those encountered during infection or cancer, and can contribute to the immunosuppressive microenvironment found in tumors.

Dysregulation of Tregs has been implicated in various autoimmune diseases, including type 1 diabetes, rheumatoid arthritis, and multiple sclerosis, as well as in cancer and infectious diseases. Therefore, understanding the mechanisms that regulate Treg function is an important area of research with potential therapeutic implications.

Interleukin-23 (IL-23) is a pro-inflammatory cytokine, which is a type of signaling molecule used for communication between cells in the immune system. It is a heterodimeric protein composed of two subunits: p19 and p40. IL-23 plays a crucial role in the adaptive immune response by promoting the differentiation and activation of T-cells, particularly Th17 cells, which are involved in inflammatory responses.

IL-23 is produced primarily by activated dendritic cells and macrophages in response to various stimuli such as pathogens or tissue damage. Dysregulation of IL-23 has been implicated in several autoimmune diseases, including psoriasis, inflammatory bowel disease, rheumatoid arthritis, and multiple sclerosis. Therefore, therapeutic strategies targeting IL-23 are being explored as potential treatments for these conditions.

T-box domain proteins are a family of transcription factors that share a highly conserved DNA-binding domain, known as the T-box. The T-box domain is a DNA-binding motif that specifically recognizes and binds to T-box binding elements (TBEs) in the regulatory regions of target genes. These proteins play crucial roles during embryonic development, particularly in the formation of specific tissues and organs, such as the heart, limbs, and brain. Mutations in T-box domain proteins can lead to various congenital defects and developmental disorders. Some examples of T-box domain proteins include TBX1, TBX5, and TBX20.

Immunologic adjuvants are substances that are added to a vaccine to enhance the body's immune response to the antigens contained in the vaccine. They work by stimulating the immune system and promoting the production of antibodies and activating immune cells, such as T-cells and macrophages, which help to provide a stronger and more sustained immune response to the vaccine.

Immunologic adjuvants can be derived from various sources, including bacteria, viruses, and chemicals. Some common examples include aluminum salts (alum), oil-in-water emulsions (such as MF59), and bacterial components (such as lipopolysaccharide or LPS).

The use of immunologic adjuvants in vaccines can help to improve the efficacy of the vaccine, particularly for vaccines that contain weak or poorly immunogenic antigens. They can also help to reduce the amount of antigen needed in a vaccine, which can be beneficial for vaccines that are difficult or expensive to produce.

It's important to note that while adjuvants can enhance the immune response to a vaccine, they can also increase the risk of adverse reactions, such as inflammation and pain at the injection site. Therefore, the use of immunologic adjuvants must be carefully balanced against their potential benefits and risks.

The spleen is an organ in the upper left side of the abdomen, next to the stomach and behind the ribs. It plays multiple supporting roles in the body:

1. It fights infection by acting as a filter for the blood. Old red blood cells are recycled in the spleen, and platelets and white blood cells are stored there.
2. The spleen also helps to control the amount of blood in the body by removing excess red blood cells and storing platelets.
3. It has an important role in immune function, producing antibodies and removing microorganisms and damaged red blood cells from the bloodstream.

The spleen can be removed without causing any significant problems, as other organs take over its functions. This is known as a splenectomy and may be necessary if the spleen is damaged or diseased.

STAT6 (Signal Transducer and Activator of Transcription 6) is a transcription factor that plays a crucial role in the immune response, particularly in the development of Th2 cells and the production of cytokines. It is activated by cytokines such as IL-4 and IL-13 through phosphorylation, which leads to its dimerization and translocation into the nucleus where it binds to specific DNA sequences and regulates the expression of target genes. STAT6 is involved in a variety of biological processes including allergic responses, inflammation, and tumorigenesis. Mutations in the STAT6 gene have been associated with immunodeficiency disorders and certain types of cancer.

Flow cytometry is a medical and research technique used to measure physical and chemical characteristics of cells or particles, one cell at a time, as they flow in a fluid stream through a beam of light. The properties measured include:

* Cell size (light scatter)
* Cell internal complexity (granularity, also light scatter)
* Presence or absence of specific proteins or other molecules on the cell surface or inside the cell (using fluorescent antibodies or other fluorescent probes)

The technique is widely used in cell counting, cell sorting, protein engineering, biomarker discovery and monitoring disease progression, particularly in hematology, immunology, and cancer research.

Adoptive transfer is a medical procedure in which immune cells are transferred from a donor to a recipient with the aim of providing immunity or treating a disease, such as cancer. This technique is often used in the field of immunotherapy and involves isolating specific immune cells (like T-cells) from the donor, expanding their numbers in the laboratory, and then infusing them into the patient. The transferred cells are expected to recognize and attack the target cells, such as malignant or infected cells, leading to a therapeutic effect. This process requires careful matching of donor and recipient to minimize the risk of rejection and graft-versus-host disease.

Immunoglobulin E (IgE) is a type of antibody that plays a key role in the immune response to parasitic infections and allergies. It is produced by B cells in response to stimulation by antigens, such as pollen, pet dander, or certain foods. Once produced, IgE binds to receptors on the surface of mast cells and basophils, which are immune cells found in tissues and blood respectively. When an individual with IgE antibodies encounters the allergen again, the cross-linking of IgE molecules bound to the FcεRI receptor triggers the release of mediators such as histamine, leukotrienes, prostaglandins, and various cytokines from these cells. These mediators cause the symptoms of an allergic reaction, such as itching, swelling, and redness. IgE also plays a role in protecting against certain parasitic infections by activating eosinophils, which can kill the parasites.

In summary, Immunoglobulin E (IgE) is a type of antibody that plays a crucial role in the immune response to allergens and parasitic infections, it binds to receptors on the surface of mast cells and basophils, when an individual with IgE antibodies encounters the allergen again, it triggers the release of mediators from these cells causing the symptoms of an allergic reaction.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

STAT4 (Signal Transducer and Activator of Transcription 4) is a transcription factor protein that plays a crucial role in the immune response. When activated, STAT4 translocates to the nucleus and binds to specific DNA sequences, regulating the expression of target genes involved in various cellular processes such as differentiation, proliferation, and activation of immune cells like T-cells.

Activation of STAT4 occurs through phosphorylation by receptor associated kinases, following cytokine stimulation, particularly interleukin (IL)-12 and type I interferons. Once activated, STAT4 forms homodimers or heterodimers with other STAT proteins, which then translocate to the nucleus and bind to specific DNA sequences called gamma-activated sites (GAS) in the promoter regions of target genes.

Mutations in the STAT4 gene have been associated with various autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis, highlighting its importance in maintaining immune homeostasis.

Autoimmune encephalomyelitis (EAE) is a model of inflammatory demyelinating disease used in medical research to study the mechanisms of multiple sclerosis (MS) and develop new therapies. It is experimentally induced in laboratory animals, typically mice or rats, through immunization with myelin antigens or T-cell transfer. The resulting immune response leads to inflammation, demyelination, and neurological dysfunction in the central nervous system (CNS), mimicking certain aspects of MS.

EAE is a valuable tool for understanding the pathogenesis of MS and testing potential treatments. However, it is essential to recognize that EAE is an experimental model and may not fully recapitulate all features of human autoimmune encephalomyelitis.

An allergen is a substance that can cause an allergic reaction in some people. These substances are typically harmless to most people, but for those with allergies, the immune system mistakenly identifies them as threats and overreacts, leading to the release of histamines and other chemicals that cause symptoms such as itching, sneezing, runny nose, rashes, hives, and difficulty breathing. Common allergens include pollen, dust mites, mold spores, pet dander, insect venom, and certain foods or medications. When a person comes into contact with an allergen, they may experience symptoms that range from mild to severe, depending on the individual's sensitivity to the substance and the amount of exposure.

No FAQ available that match "th1 cells"

No images available that match "th1 cells"