Lymphotoxin beta Receptor
Lymphotoxin-beta
Lymphotoxin-alpha
Tumor Necrosis Factor Ligand Superfamily Member 14
Lymphotoxin alpha1, beta2 Heterotrimer
Receptors, Tumor Necrosis Factor
Receptors, Tumor Necrosis Factor, Member 14
Lymphoid Tissue
NF-kappa B p52 Subunit
Dendritic Cells, Follicular
Chemokine CCL21
Receptors, Tumor Necrosis Factor, Type I
Tumor Necrosis Factor-alpha
Transcription Factor RelB
Mice, Knockout
Mice, Inbred C57BL
Membrane Proteins
Signal Transduction
NF-kappa B
Interleukin-1beta
Encyclopedias as Topic
Lymph node germinal centers form in the absence of follicular dendritic cell networks. (1/107)
Follicular dendritic cell networks are said to be pivotal to both the formation of germinal centers (GCs) and their functions in generating antigen-specific antibody affinity maturation and B cell memory. We report that lymphotoxin beta-deficient mice form GC cell clusters in the gross anatomical location expected of GCs, despite the complete absence of follicular dendritic cell networks. Furthermore, antigen-specific GC generation was at first relatively normal, but these GCs then rapidly regressed and GC-phase antibody affinity maturation was reduced. Lymphotoxin beta-deficient mice also showed substantial B cell memory in their mesenteric lymph nodes. This memory antibody response was of relatively low affinity for antigen at week 4 after challenge, but by week 10 after challenge was comparable to wild-type, indicating that affinity maturation had failed in the GC phase but developed later. (+info)Expression of the lymphotoxin beta receptor on follicular stromal cells in human lymphoid tissues. (2/107)
The lymphotoxin beta receptor (LTbetaR), and its ligand, LTalpha1beta2, have been proposed to play a key role in the development and organization of lymphoid tissues. The LTbetaR is expressed on a variety of human primary and transformed cells, but strikingly absent on T or B lymphocytes and primary monocytes or peripheral dendritic cells, although LTbetaR is detected on some myeloid leukemic lines. In the developing thymus LTbetaR is prominent along the trabeculae and into the medulla upto corticomedullary junction. In the spleen, LTbetaR is prominently expressed by cells in the red pulp and along the borders of red and white pulp which colocalizes with reticular stromal cells. The LTbetaR is expressed on a human follicular dendritic cell line, FDC-1, and signals expression of CD54 when ligated with the LTalpha1beta2 complex. These results support the concept that directional interactions between LTalpha1beta2 bearing lymphocytes and LTbetaR bearing stromal cells are involved in the organization of lymphoid tissue. (+info)Lymphotoxin-beta-deficient mice show defective antiviral immunity. (3/107)
Lymphotoxin beta (LTbeta), a member of the tumor necrosis factor family, plays an important role in lymphoid organogenesis. In order to determine whether LTbeta is involved in cellular immunity, we investigated the antiviral immune response of LTbeta-deficient (LTbeta -/-) mice to lymphocytic choriomeningitis virus (LCMV). Cytotoxic T lymphocyte (CTL) responses to LCMV were severely diminished, leading to viral persistence in brain and kidney. However, major functions of LTbeta-deficient T lymphocytes and dendritic cells were intact. Reconstitution of irradiated LTbeta +/+ mice with LTbeta -/- bone marrow induced a disorganized splenic structure, accompanied by impairment of the LCMV-specific CTL response. These data indicate that the absence of LTbeta does not affect the intrinsic function of T lymphocytes or of dendritic cells but that the structural integrity of the spleen is strongly associated with generation of antiviral immunity. (+info)Constitutive expression and role of the TNF family ligands in apoptotic killing of tumor cells by human NK cells. (4/107)
Natural killer cells mediate spontaneously secretory/necrotic killing against rare leukemia cell lines and a nonsecretory/apoptotic killing against a large variety of tumor cell lines. The molecules involved in nonsecretory/apoptotic killing are largely undefined. In the present study, freshly isolated, nonactivated, human NK cells were shown to express TNF, lymphotoxin (LT)-alpha, LT-beta, Fas ligand (L), CD27L, CD30L, OX40L, 4-1BBL, and TNF-related apoptosis-inducing ligand (TRAIL), but not CD40L or nerve growth factor. Complementary receptors were demonstrated to be expressed on the cell surface of solid tumor cell lines susceptible to apoptotic killing mediated by NK cells. Individually applied, antagonists of TNF, LT-alpha1beta2, or FasL fully inhibited NK cell-mediated apoptotic killing of tumor cells. On the other hand, recombinant TNF, LT-alpha1beta2, or FasL applied individually or as pairs were not cytotoxic. In contrast, a mixture of the three ligands mediated significant apoptosis in tumor cells. These findings demonstrate that human NK cells constitutively express several of the TNF family ligands and induce apoptosis in tumor cells by simultaneous engagement of at least three of these cytotoxic molecules. (+info)TNF and lymphotoxin beta cooperate in the maintenance of secondary lymphoid tissue microarchitecture but not in the development of lymph nodes. (5/107)
Inactivation of genes encoding members of TNF and TNF receptor families reveal their divergent roles in the formation and function of secondary lymphoid organs. Most lymphotoxin alpha (ltalpha)- and all lymphotoxin beta receptor (ltbetar)-deficient mice are completely devoid of lymph nodes (LNs); however, most lymphotoxin beta (ltbeta)-deficient mice develop mesenteric LNs. Tnf- and tnfrp55-deficient mice develop a complete set of LNs, while ltbeta/tnfrp55 double-deficient mice lack all LNs, demonstrating cooperation between LTbeta and TNFRp55 in LN development. Now we report that ltbeta/tnf double-deficient mice develop the same set of mucosal LNs as do ltbeta-deficient mice, suggesting that ligands other than TNF signal through TNFRp55 during LN development. These LNs retain distinct T and B cells areas; however, they lack follicular dendritic cell networks. Structures resembling germinal centers can be found in the LNs from immunized ltbeta-deficient mice but not in ltbeta/tnf double-deficient mice. Additionally, stromal components of the spleen and LNs appear to be more severely disturbed in ltbeta/tnf double-deficient mice as compared with ltbeta-deficient mice. We conclude that LTbeta and TNF cooperate in the establishment of the correct microarchitecture of lymphoid organs. (+info)Lymphoid tissue homing chemokines are expressed in chronic inflammation. (6/107)
Secondary lymphoid tissue chemokine (SLC) and B lymphocyte chemoattractant (BLC) are homing chemokines that have been implicated in the trafficking of lymphocytes and dendritic cells in lymphoid organs. Lymphotoxin-alpha (LTalpha), a cytokine crucial for development of lymphoid organs, is important for expression of SLC and BLC in secondary lymphoid organs during development. Here we report that transgenic expression of LTalpha induces inflammation and ectopic expression of SLC and BLC in the adult animal. LTbeta was not necessary for induction of BLC and SLC in inflamed tissues, whereas, in contrast, tumor necrosis factor receptor-1 was found to be important for the LTalpha-mediated induction of these chemokines. The ectopic expression of LTalpha is associated with a chronic inflammation that closely resembles organized lymphoid tissue and this lymphoid neogenesis can also be seen in several chronic inflammatory diseases, including in the pancreas of the prediabetic nonobese diabetic (NOD) mouse. Expression of SLC was also observed in the pancreas of prediabetic NOD mice. This study implicates BLC and SLC in chronic inflammation and presents further evidence that LTalpha orchestrates lymphoid organogenesis both during development and in inflammatory processes. (+info)Alternate mucosal immune system: organized Peyer's patches are not required for IgA responses in the gastrointestinal tract. (7/107)
The progeny of mice treated with lymphotoxin (LT)-beta receptor (LTbetaR) and Ig (LTbetaR-Ig) lack Peyer's patches but not mesenteric lymph nodes (MLN). In this study, we used this approach to determine the importance of Peyer's patches for induction of mucosal IgA Ab responses in the murine gastrointestinal tract. Immunohistochemical analysis revealed that LTbetaR-Ig-treated, Peyer's patch null (PP null) mice possessed significant numbers of IgA-positive (IgA+) plasma cells in the intestinal lamina propria. Further, oral immunization of PP null mice with OVA plus cholera toxin as mucosal adjuvant resulted in Ag-specific mucosal IgA and serum IgG Ab responses. OVA-specific CD4+ T cells of the Th2 type were induced in MLN and spleen of PP null mice. In contrast, when TNF and LT-alpha double knockout (TNF/LT-alpha-/-) mice, which lack both Peyer's patches and MLN, were orally immunized with OVA plus cholera toxin, neither mucosal IgA nor serum IgG anti-OVA Abs were induced. On the other hand, LTbetaR-Ig- and TNF receptor 55-Ig-treated normal adult mice elicited OVA- and cholera toxin B subunit-specific mucosal IgA responses, indicating that both LT-alphabeta and TNF/LT-alpha pathways do not contribute for class switching for IgA Ab responses. These results show that the MLN plays a more important role than had been appreciated until now for the induction of both mucosal and systemic Ab responses after oral immunization. Further, organized Peyer's patches are not a strict requirement for induction of mucosal IgA Ab responses in the gastrointestinal tract. (+info)Membrane lymphotoxin is required for the development of different subpopulations of NK T cells. (8/107)
The development of lymphoid organs requires membrane-bound lymphotoxin (LT), a heterotrimer containing LTalpha and LTbeta, but the effects of LT on T cell function have not been characterized extensively. Upon TCR cross-linking in vitro, splenocytes from both LTalpha-/- and LTbeta-/- mice failed to produce IL-4 and IL-10 due to a reduction in NK T cells. Concordantly, LTalpha-/- and LTbeta-/- mice did not respond to the lipoglycan alpha-galactosylceramide, which is presented by mouse CD1 to Valpha14+ NK T cells. Interestingly, both populations of NK T cells, including those that are mouse CD1 dependent and alpha-galactosylceramide reactive and those that are not, were affected by disruption of the LTalpha and LTbeta genes. NK T cells were not affected, however, in transgenic mice in which LT signaling is blocked, beginning on day 3 after birth, by expression of a soluble decoy LTbeta receptor. This suggests that membrane-bound LT is critical for NK T cells early in ontogeny, but not for the homeostasis of mature cells. (+info)The Lymphotoxin-beta receptor (LTβR) is a type III transmembrane protein and a member of the tumor necrosis factor receptor superfamily (TNFRSF). It is primarily expressed on the surface of various cell types, including immune cells such as lymphocytes, dendritic cells, and stromal cells in lymphoid organs.
LTβR binds to its ligands, Lymphotoxin-alpha (LTα) and Lymphotoxin-beta (LTβ), which are primarily produced by activated T-cells and B-cells. The binding of LTα/LTβ to LTβR triggers a signaling cascade that leads to the activation of various downstream signaling pathways, including NF-κB and MAPK pathways.
The activation of LTβR plays critical roles in the development and organization of lymphoid tissues, immune responses, and inflammation. Dysregulation of LTβR signaling has been implicated in various autoimmune diseases, such as rheumatoid arthritis, inflammatory bowel disease, and multiple sclerosis.
Lymphotoxin-beta (LT-β) is a cytokine that belongs to the tumor necrosis factor (TNF) family. It is primarily produced by activated T lymphocytes and plays an essential role in the development and organization of the immune system, particularly in the formation of lymphoid structures such as lymph nodes and Peyer's patches.
LT-β forms a complex with its receptor, LTβR, which is expressed on various cell types including stromal cells, endothelial cells, and immune cells. The binding of LT-β to LTβR triggers a cascade of intracellular signaling events that lead to the activation of genes involved in the development and maintenance of lymphoid tissues.
In addition to its role in lymphoid organogenesis, LT-β has been implicated in various immune responses, including inflammation, immune cell recruitment, and the regulation of adaptive immunity. Dysregulation of LT-β signaling has been associated with several autoimmune diseases, making it a potential target for therapeutic intervention.
Lymphotoxin-alpha (LT-alpha), also known as Tumor Necrosis Factor-beta (TNF-beta), is a cytokine that belongs to the TNF superfamily. It is primarily produced by activated CD4+ and CD8+ T cells, and to some extent by B cells, natural killer (NK) cells, and neutrophils. LT-alpha can form homotrimers or heterotrimers with Lymphotoxin-beta (LT-beta), which bind to the LT-beta receptor (LTβR) and herceptin-resistant tumor cells (HRT) on the surface of various cell types, including immune cells, fibroblasts, and endothelial cells.
The activation of the LTβR signaling pathway plays a crucial role in the development and organization of secondary lymphoid organs, such as lymph nodes, Peyer's patches, and spleen. Additionally, LT-alpha has proinflammatory effects, inducing apoptosis in susceptible cells, activating immune cells, and contributing to the pathogenesis of several inflammatory diseases, including rheumatoid arthritis, psoriasis, and Crohn's disease.
Tumor Necrosis Factor Ligand Superfamily Member 14 (TNFSF14), also known as HVEM (Herpesvirus Entry Mediator) Ligand or Lymphotoxin-like, Inhibitory or Secreting Factor (LIGHT), is a type II transmembrane protein and a member of the Tumor Necrosis Factor (TNF) ligand superfamily. It plays a crucial role in immune cell communication and regulation of inflammatory responses.
TNFSF14 can exist as both a membrane-bound form and a soluble form, produced through proteolytic cleavage or alternative splicing. The protein interacts with two receptors: HVEM (TNFRSF14) and Lymphotoxin β Receptor (LTβR). Depending on the receptor it binds to, TNFSF14 can have either costimulatory or inhibitory effects on immune cell functions.
The binding of TNFSF14 to HVEM promotes the activation and proliferation of T cells, enhances the cytotoxic activity of natural killer (NK) cells, and contributes to the development and maintenance of secondary lymphoid organs. In contrast, the interaction between TNFSF14 and LTβR primarily induces the formation and remodeling of tertiary lymphoid structures in peripheral tissues during inflammation or infection.
Dysregulation of TNFSF14 has been implicated in various pathological conditions, including autoimmune diseases, chronic inflammation, and cancer. Therefore, targeting this molecule and its signaling pathways is an area of interest for developing novel therapeutic strategies to treat these disorders.
Lymphotoxin-alpha1, beta2 heterotrimer (LT-alpha1/beta2) is not typically defined in the context of medical terminology. However, it is a term used to describe a specific form of lymphotoxin, which is a cytokine involved in the immune response.
Lymphotoxins are a type of tumor necrosis factor (TNF) that can induce apoptosis (programmed cell death) in certain cells. They exist in two forms: LT-alpha and LT-beta, which can combine to form heterotrimers (LT-alpha1/beta2) or homotrimers (LT-alpha3 or LT-beta3).
The LT-alpha1/beta2 heterotrimer is a transmembrane protein complex composed of one alpha and two beta subunits. It plays an important role in the development and maintenance of lymphoid tissue, including the formation of germinal centers in lymph nodes and Peyer's patches.
In summary, while not a strictly medical definition, Lymphotoxin-alpha1, beta2 heterotrimer refers to a specific form of lymphotoxin that plays a crucial role in the immune response by contributing to the development and maintenance of lymphoid tissue.
Tumor Necrosis Factor (TNF) Receptors are cell surface receptors that bind to tumor necrosis factor cytokines. They play crucial roles in the regulation of a variety of immune cell functions, including inflammation, immunity, and cell survival or death (apoptosis).
There are two major types of TNF receptors: TNFR1 (also known as p55 or CD120a) and TNFR2 (also known as p75 or CD120b). TNFR1 is widely expressed in most tissues, while TNFR2 has a more restricted expression pattern and is mainly found on immune cells.
TNF receptors have an intracellular domain called the death domain, which can trigger signaling pathways leading to apoptosis when activated by TNF ligands. However, they can also activate other signaling pathways that promote cell survival, differentiation, and inflammation. Dysregulation of TNF receptor signaling has been implicated in various diseases, including cancer, autoimmune disorders, and neurodegenerative conditions.
Tumor necrosis factor receptor superfamily member 14 (TNFRSF14), also known as HVEM (herpesvirus entry mediator), is a type of cell surface receptor that belongs to the tumor necrosis factor receptor superfamily. It is involved in various immune responses and can be found on the surface of different types of cells, including T cells, B cells, and myeloid cells.
TNFRSF14 has been shown to interact with several ligands, including LIGHT (TNFSF14) and BTLA (B- and T-lymphocyte attenuator), which can either activate or inhibit immune responses. The interaction between TNFRSF14 and its ligands plays a crucial role in regulating the activation, proliferation, and effector functions of immune cells.
In the context of tumors, TNFRSF14 has been found to be expressed on some tumor cells, where it can contribute to tumor growth and progression by promoting immune evasion and resistance to therapies. Additionally, genetic variations in TNFRSF14 have been associated with susceptibility to certain autoimmune diseases, such as rheumatoid arthritis and systemic lupus erythematosus.
Overall, TNFRSF14 is a critical regulator of immune responses and has important implications for the development of cancer and autoimmune diseases.
Lymphoid tissue is a specialized type of connective tissue that is involved in the immune function of the body. It is composed of lymphocytes (a type of white blood cell), which are responsible for producing antibodies and destroying infected or cancerous cells. Lymphoid tissue can be found throughout the body, but it is particularly concentrated in certain areas such as the lymph nodes, spleen, tonsils, and Peyer's patches in the small intestine.
Lymphoid tissue provides a site for the activation, proliferation, and differentiation of lymphocytes, which are critical components of the adaptive immune response. It also serves as a filter for foreign particles, such as bacteria and viruses, that may enter the body through various routes. The lymphatic system, which includes lymphoid tissue, helps to maintain the health and integrity of the body by protecting it from infection and disease.
NF-κB (Nuclear Factor kappa-light-chain-enhancer of activated B cells) is a protein complex that regulates many normal cellular and inflammatory responses, including cell survival, differentiation, and apoptosis. NF-κB p52 subunit is one of the several subunits that make up this protein complex.
The p52 subunit is derived from the proteolytic processing of its precursor protein, p100. This process occurs in response to certain stimuli and results in the formation of a mature p52 subunit, which then combines with other NF-κB family members (such as RelB) to form a functional NF-κB heterodimer.
The activated NF-κB complex then translocates to the nucleus, where it binds to specific DNA sequences called κB sites and regulates the expression of target genes involved in various cellular processes, such as immune response, inflammation, differentiation, and stress responses. Dysregulation of NF-κB signaling has been implicated in several diseases, including cancer, autoimmune disorders, and chronic inflammatory conditions.
Follicular dendritic cells (FDCs) are a specialized type of dendritic cell that reside in the germinal centers of secondary lymphoid organs, such as the spleen, lymph nodes, and Peyer's patches. They play a critical role in the adaptive immune response by presenting antigens to B cells and helping to regulate their activation, differentiation, and survival.
FDCs are characterized by their extensive network of dendrites, which can trap and retain antigens on their surface for extended periods. They also express a variety of surface receptors that allow them to interact with other immune cells, including complement receptors, Fc receptors, and cytokine receptors.
FDCs are derived from mesenchymal stem cells and are distinct from classical dendritic cells, which are derived from hematopoietic stem cells. They are long-lived cells that can survive for months or even years in the body, making them important players in the maintenance of immune memory.
Overall, follicular dendritic cells play a critical role in the adaptive immune response by helping to regulate B cell activation and differentiation, and by contributing to the development of immune memory.
Chemokine (C-C motif) ligand 21 (CCL21), also known as secondary lymphoid tissue chemokine (SLC) or exodus-2, is a type of chemokine that belongs to the CC subfamily. Chemokines are small signaling proteins that play crucial roles in regulating immune responses and inflammation by recruiting various leukocytes to sites of infection or injury through specific receptor binding.
CCL21 is primarily expressed in high endothelial venules (HEVs) within lymphoid tissues, such as lymph nodes, spleen, and Peyer's patches. It functions as a chemoattractant for immune cells like dendritic cells, T cells, and B cells, guiding them to enter the HEVs and migrate into the lymphoid organs. This process is essential for initiating adaptive immune responses against pathogens or antigens.
CCL21 exerts its effects by binding to chemokine receptors CCR7 and atypical chemokine receptor ACKR3 (also known as CXCR7). The interaction between CCL21 and these receptors triggers intracellular signaling cascades, leading to cell migration and activation. Dysregulation of CCL21 expression or function has been implicated in various pathological conditions, including autoimmune diseases, cancer, and inflammatory disorders.
Peyer's patches are specialized lymphoid nodules found in the mucosa of the ileum, a part of the small intestine. They are a component of the immune system and play a crucial role in monitoring and defending against harmful pathogens that are ingested with food and drink. Peyer's patches contain large numbers of B-lymphocytes, T-lymphocytes, and macrophages, which work together to identify and eliminate potential threats. They also have a unique structure that allows them to sample and analyze the contents of the intestinal lumen, providing an early warning system for the immune system.
Tumor Necrosis Factor Receptor 1 (TNFR1), also known as p55 or CD120a, is a type I transmembrane protein that belongs to the tumor necrosis factor receptor superfamily. It is widely expressed in various tissues and cells, including immune cells, endothelial cells, and fibroblasts. TNFR1 plays a crucial role in regulating inflammation, immunity, cell survival, differentiation, and apoptosis (programmed cell death).
TNFR1 is activated by its ligand, Tumor Necrosis Factor-alpha (TNF-α), which is a potent proinflammatory cytokine produced mainly by activated macrophages and monocytes. Upon binding of TNF-α to TNFR1, a series of intracellular signaling events are initiated through the recruitment of adaptor proteins, such as TNF receptor-associated death domain (TRADD), receptor-interacting protein kinase 1 (RIPK1), and TNF receptor-associated factor 2 (TRAF2). These interactions lead to the activation of several downstream signaling pathways, including nuclear factor kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs), which ultimately regulate gene expression and cellular responses.
TNFR1 has been implicated in various physiological and pathological processes, such as inflammation, infection, autoimmunity, cancer, and neurodegenerative disorders. Dysregulation of TNFR1 signaling can contribute to the development and progression of several diseases, making it an attractive target for therapeutic interventions.
Tumor Necrosis Factor-alpha (TNF-α) is a cytokine, a type of small signaling protein involved in immune response and inflammation. It is primarily produced by activated macrophages, although other cell types such as T-cells, natural killer cells, and mast cells can also produce it.
TNF-α plays a crucial role in the body's defense against infection and tissue injury by mediating inflammatory responses, activating immune cells, and inducing apoptosis (programmed cell death) in certain types of cells. It does this by binding to its receptors, TNFR1 and TNFR2, which are found on the surface of many cell types.
In addition to its role in the immune response, TNF-α has been implicated in the pathogenesis of several diseases, including autoimmune disorders such as rheumatoid arthritis, inflammatory bowel disease, and psoriasis, as well as cancer, where it can promote tumor growth and metastasis.
Therapeutic agents that target TNF-α, such as infliximab, adalimumab, and etanercept, have been developed to treat these conditions. However, these drugs can also increase the risk of infections and other side effects, so their use must be carefully monitored.
Transcription factor RelB is a member of the NF-κB (nuclear factor kappa B) family, which plays a crucial role in regulating immune responses, cell survival, and inflammation. RelB forms a heterodimer with other NF-κB family members, such as p50 or p52, and binds to specific DNA sequences called κB sites in the promoter regions of target genes. This binding leads to the activation or repression of gene transcription, ultimately influencing various cellular processes, including immune response regulation, development, and oncogenesis. RelB is unique among NF-κB family members because it can shuttle between the cytoplasm and nucleus even in unstimulated cells, although its activity is enhanced upon stimulation by various signals.
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.
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.
Membrane proteins are a type of protein that are embedded in the lipid bilayer of biological membranes, such as the plasma membrane of cells or the inner membrane of mitochondria. These proteins play crucial roles in various cellular processes, including:
1. Cell-cell recognition and signaling
2. Transport of molecules across the membrane (selective permeability)
3. Enzymatic reactions at the membrane surface
4. Energy transduction and conversion
5. Mechanosensation and signal transduction
Membrane proteins can be classified into two main categories: integral membrane proteins, which are permanently associated with the lipid bilayer, and peripheral membrane proteins, which are temporarily or loosely attached to the membrane surface. Integral membrane proteins can further be divided into three subcategories based on their topology:
1. Transmembrane proteins, which span the entire width of the lipid bilayer with one or more alpha-helices or beta-barrels.
2. Lipid-anchored proteins, which are covalently attached to lipids in the membrane via a glycosylphosphatidylinositol (GPI) anchor or other lipid modifications.
3. Monotopic proteins, which are partially embedded in the membrane and have one or more domains exposed to either side of the bilayer.
Membrane proteins are essential for maintaining cellular homeostasis and are targets for various therapeutic interventions, including drug development and gene therapy. However, their structural complexity and hydrophobicity make them challenging to study using traditional biochemical methods, requiring specialized techniques such as X-ray crystallography, nuclear magnetic resonance (NMR) spectroscopy, and single-particle cryo-electron microscopy (cryo-EM).
Signal transduction is the process by which a cell converts an extracellular signal, such as a hormone or neurotransmitter, into an intracellular response. This involves a series of molecular events that transmit the signal from the cell surface to the interior of the cell, ultimately resulting in changes in gene expression, protein activity, or metabolism.
The process typically begins with the binding of the extracellular signal to a receptor located on the cell membrane. This binding event activates the receptor, which then triggers a cascade of intracellular signaling molecules, such as second messengers, protein kinases, and ion channels. These molecules amplify and propagate the signal, ultimately leading to the activation or inhibition of specific cellular responses.
Signal transduction pathways are highly regulated and can be modulated by various factors, including other signaling molecules, post-translational modifications, and feedback mechanisms. Dysregulation of these pathways has been implicated in a variety of diseases, including cancer, diabetes, and neurological disorders.
NF-κB (Nuclear Factor kappa-light-chain-enhancer of activated B cells) is a protein complex that plays a crucial role in regulating the immune response to infection and inflammation, as well as in cell survival, differentiation, and proliferation. It is composed of several subunits, including p50, p52, p65 (RelA), c-Rel, and RelB, which can form homodimers or heterodimers that bind to specific DNA sequences called κB sites in the promoter regions of target genes.
Under normal conditions, NF-κB is sequestered in the cytoplasm by inhibitory proteins known as IκBs (inhibitors of κB). However, upon stimulation by various signals such as cytokines, bacterial or viral products, and stress, IκBs are phosphorylated, ubiquitinated, and degraded, leading to the release and activation of NF-κB. Activated NF-κB then translocates to the nucleus, where it binds to κB sites and regulates the expression of target genes involved in inflammation, immunity, cell survival, and proliferation.
Dysregulation of NF-κB signaling has been implicated in various pathological conditions such as cancer, chronic inflammation, autoimmune diseases, and neurodegenerative disorders. Therefore, targeting NF-κB signaling has emerged as a potential therapeutic strategy for the treatment of these diseases.
Interleukin-1 beta (IL-1β) is a member of the interleukin-1 cytokine family and is primarily produced by activated macrophages in response to inflammatory stimuli. It is a crucial mediator of the innate immune response and plays a key role in the regulation of various biological processes, including cell proliferation, differentiation, and apoptosis. IL-1β is involved in the pathogenesis of several inflammatory diseases, such as rheumatoid arthritis, inflammatory bowel disease, and atherosclerosis. It exerts its effects by binding to the interleukin-1 receptor, which triggers a signaling cascade that leads to the activation of various transcription factors and the expression of target genes.
An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.
Ectopic hormone production refers to the situation when a hormone is produced in an unusual location or by a type of cell that does not typically produce it. This can occur due to various reasons such as genetic mutations, cancer, or other medical conditions. The ectopic hormone production can lead to hormonal imbalances and related symptoms, as the regulation of hormones in the body becomes disrupted.
For example, in some cases of lung cancer, the tumor cells may produce adrenocorticotropic hormone (ACTH), which is typically produced by the pituitary gland. This ectopic ACTH production can result in Cushing's syndrome, a condition characterized by symptoms such as weight gain, muscle weakness, and high blood pressure.
It's important to note that ectopic hormone production is relatively rare and usually occurs in the context of specific medical conditions. If you suspect that you or someone else may have ectopic hormone production, it's important to seek medical attention from a healthcare professional who can provide appropriate evaluation and treatment.
Lymphotoxin beta
Lymphotoxin beta receptor
Lymphotoxin alpha
Lymphotoxin
Sergio A. Lira
TRAF3
Galectin-2
High endothelial venules
LIGHT (protein)
TRAF5
Diet-induced obesity model
Diablo homolog
TRAF2
Baculoviral IAP repeat-containing protein 2
TANK (gene)
MAP3K8
MAP3K14
CHUK
IKK2
GPR183
Peptic ulcer disease
Macrophage
LTB
LTBR
List of MeSH codes (D12.776)
B cell growth and differentiation factors
Infliximab
Index of immunology articles
Pathology of multiple sclerosis
List of MeSH codes (D12.644)
Lymphotoxin beta - Wikipedia
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Receptor6
- The predominant form on the lymphocyte surface is the lymphotoxin-alpha 1/beta 2 complex (e.g. 1 molecule alpha/2 molecules beta) and this complex is the primary ligand for the lymphotoxin-beta receptor. (wikipedia.org)
- NF-kappaB-inducing kinase is dispensable for activation of NF-kappaB in inflammatory settings but essential for lymphotoxin beta receptor activation of NF-kappaB in primary human fibroblasts. (ox.ac.uk)
- Does not cross-react with TNF-beta, lymphotoxin and receptor bound TNF-alpha. (lsbio.com)
- Human Lymphotoxin beta receptor (L Tbeta R, TNFRSF3) is a member of the TNF receptor superfamily with similarilty to CD120a(TNFR1) and CD120b(TNFR2). (ancell.com)
- By employing single-cell transcriptomics, endothelial fate mapping, and functional multiplex immune profiling, we demonstrate that antiangiogenic immune-modulating therapies evoke transdifferentiation of postcapillary venules into inflamed high-endothelial venules (HEVs) via lymphotoxin/lymphotoxin beta receptor (LT/LTβR) signaling. (utu.fi)
- The lymphotoxin beta receptor (LTβR) belongs to the TNF receptor superfamily and is essential for the organogenesis of secondary lymphoid organs as well as the coordination of an effective immune response against invading pathogens. (sfi-dgfi-2023.fr)
Tumor necros3
- Lymphotoxin-beta (LT-beta) also known as tumor necrosis factor C (TNF-C) is a protein that in humans is encoded by the LTB gene. (wikipedia.org)
- Lymphotoxin-alpha (LT-α) or tumor necrosis factor-beta (TNF-β) is a protein that in humans is encoded by the LTA gene . (wikidoc.org)
- Lymphotoxin alpha, a member of the tumor necrosis factor family , is a cytokine produced by lymphocytes . (wikidoc.org)
Heterotrimers2
- LT-α can also form heterotrimers with lymphotoxin-beta , which anchors lymphotoxin-alpha to the cell surface. (wikidoc.org)
- TNF-β forms heterotrimers with lymphotoxin-beta, which anchors TNF-β to the cell surface. (novoprolabs.com)
Anchors1
- It anchors lymphotoxin-alpha to the cell surface through heterotrimer formation. (wikipedia.org)
Gene3
- However, these studies utilized mice with complete LTα gene deficiency that did not allow to distinguish effects of soluble versus membrane-associated LT. LTB has been shown to interact with Lymphotoxin alpha. (wikipedia.org)
- Association of tumor necrosis factors-beta gene polymorphism with endometriosis in women in Guangdong Province]. (cdc.gov)
- Effect of gene polymorphism of TNF-beta on the concentration of TNF in serum of patient with endometriosis]. (cdc.gov)
Lymphocytes1
- TNF-beta, or lymphotoxin, is produced by lymphocytes. (medscape.com)
Membrane1
- Lymphotoxin beta is a type II membrane protein of the TNF family. (wikipedia.org)
Serum4
- Description: A sandwich quantitative ELISA assay kit for detection of Mouse Lymphotoxin Beta (LTb) in samples from serum, plasma, tissue homogenates, cell lysates or other biological fluids. (hudsen.org)
- Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Mouse Lymphotoxin Beta (LTb) in serum, plasma, tissue homogenates, cell lysates and other biological fluids. (hudsen.org)
- Description: Enzyme-linked immunosorbent assay based on the Double-antibody Sandwich method for detection of Mouse Lymphotoxin Beta (LTb) in samples from serum, plasma, tissue homogenates, cell lysates and other biological fluids with no significant corss-reactivity with analogues from other species. (hudsen.org)
- Description: A sandwich ELISA kit for detection of Lymphotoxin Beta from Mouse in samples from blood, serum, plasma, cell culture fluid and other biological fluids. (hudsen.org)
Alpha4
- The minor complex is lymphotoxin-alpha 2/beta 1. (wikipedia.org)
- Lymphotoxin-beta isoform b is unable to complex with lymphotoxin-alpha suggesting a function for lymphotoxin-beta which is independent of lymphotoxin-alpha. (wikipedia.org)
- Using an adenoviral vector encoding kinase-deficient NIK, we have investigated the role of NIK in LPS, IL-1, TNF-alpha, and lymphotoxin (LT) betaR signaling in primary human cells and TNF-alpha expression from rheumatoid tissue. (ox.ac.uk)
- Histological changes in the trachea were accompanied by increased mRNA expression of interleukin (IL)-4, tumour necrosis factor alpha, lymphotoxin beta, lymphotactin and Rantes, as well as TDI-specific IgG antibodies and elevated levels of total IgE. (cdc.gov)
Symbol1
- actin beta [Source:HGNC Symbol;Acc:HGN. (gsea-msigdb.org)
Function1
- and inhibition of neurofibromatosis (NF)-kappa-beta function. (medscape.com)
Expression1
- Moreover we found that expression of Ltb (encoding lymphotoxin b), Areg (encoding amphiregulin) a. (achrinhibitor.com)
Forms1
- Characterization of surface lymphotoxin forms. (wikipedia.org)
Shown1
- In experimental cerebral malaria, TNF-beta, now called lymphotoxin α (LT), has been shown to be a principal mediator of pathogenesis. (plos.org)
Factor2
- the latter include transforming growth factor beta (TGF-β), interleukin-6 (IL-6), IL-8, IL-11, nerve growth factor (NGF), insulin-like growth factor-I (IGF-I) and IGF-II. (ox.ac.uk)
- Genetic variation in tumour necrosis factor and lymphotoxin is not associated with endometriosis in an Australian sample. (cdc.gov)
Source1
- cytochrome b-245 beta chain [Source. (gsea-msigdb.org)
Tumor5
- Lymphotoxin-beta (LT-beta) also known as tumor necrosis factor C (TNF-C) is a protein that in humans is encoded by the LTB gene. (wikipedia.org)
- Using reverse transcriptase polymerase chain reaction (RT-PCR) analysis of the tumor, we found elevated levels of IL-6 mRNA as expected, but also elevated levels of tumor necrosis factor beta (TNF-beta) and gamma interferon (gamma-IFN) mRNA. (nih.gov)
- Association between lymphotoxin-(alpha) (tumor necrosis factor-(beta)) intron polymorphism and predisposition to severe sepsis is modified by gender and age. (ajbm.net)
- TNF alpha is closely related to the 25kDa protein Tumor Necrosis Factor beta (lymphotoxin), sharing the same receptors and cellular actions. (nsjbio.com)
- The human tumor necrosis factor locus (TNF locus) is located within the major histocompatibility complex between the class III genes and HLA-B. We recently characterized and studied two closely linked highly informative dinucleotide repeats (AC/GT)n (designated TNFa) and (TC/GA)k (designated TNFb) in the upstream region of the human TNF-beta (lymphotoxin) gene. (ox.ac.uk)
Superfamily1
- The non-canonical pathway is triggered by particular members of the TNFR superfamily, such as lymphotoxin-beta (LT-beta) or BAFF. (uni-freiburg.de)
Protein3
- Lymphotoxin beta is a type II membrane protein of the TNF family. (wikipedia.org)
- catenin beta interacting protein 1 [So. (gsea-msigdb.org)
- Human Beta-Tubulin 3 is a 50,432 dalton structural protein (450 amino acid) expressed in neurons of the PNS and CNS. (aveslabs.com)
Cytokines1
- Because these cytokines are mediators of immune regulation and inflammation, we propose that TNF-beta and gamma-IFN also play an important role in the pathophysiology of Castleman's disease. (nih.gov)
Tumour3
- Histological changes in the trachea were accompanied by increased mRNA expression of interleukin (IL)-4, tumour necrosis factor alpha, lymphotoxin beta, lymphotactin and Rantes, as well as TDI-specific IgG antibodies and elevated levels of total IgE. (cdc.gov)
- HLA class II induction in human islet cells by interferon-gamma plus tumour necrosis factor or lymphotoxin. (ox.ac.uk)
- The cytotoxins tumour necrosis factor (TNF) and lymphotoxin (LT) synergize with IFN-gamma in a number of activities. (ox.ac.uk)
Antibody1
- Bulk Order Inquiry for Anti-Beta-Tubulin 3 Antibody ------- (please add any order requirements, including desired quantity, timing, etc. (aveslabs.com)
Intron1
- Here, we combine these four markers together with a biallelic TC/GA repeat in the first intron of the TNF-beta gene (TNFc) and a biallelic NcoI RFLP (TNFn) to type 105 cell lines from the American Society of Histocompatibility and Immunogenetics Workshop and the Center for Human Polymorphism Studies reference panels of HLA typing cell lines. (ox.ac.uk)
Antigens1
- In type I diabetes, islet beta cells, the target of the autoimmune process, selectively express class II antigens. (ox.ac.uk)
Gamma1
- But in contrast to most other cell types, islet beta cells are not stimulated to express class II by interferon-gamma (IFN-gamma) and thus the conditions under which this induction occurs have been particularly elusive. (ox.ac.uk)
Member1
- Lymphotoxin (LT)-α, a member of the TNF family, is recognized as an important mediator in different aspects of lymphoid organ development. (edu.au)
Regulation1
- 7. RelB is required for Peyer's patch development: differential regulation of p52-RelB by lymphotoxin and TNF. (nih.gov)
Human1
- 16. Pociot F, Molvig J, Wogensen L, Worsaae H, Nerup J. A TaqI polymorphism in the human interleukin-1 beta (IL-1 beta) gene correlates with IL-1 beta secretion in vitro . (ajbm.net)
Inflammatory1
- Lymphotoxin-α (LTA) is a cytokine involved in inflammatory reactions. (edu.pl)