Interleukins
Interleukin-6
Cytokines
Interleukin-1
Interleukin-4
Interleukin-2
Interleukin-8
Interleukin-10
Tumor Necrosis Factor-alpha
Interleukin-5
Inflammation Mediators
Inflammation
Receptors, Interleukin
Cells, Cultured
Interleukin-7
T-Lymphocytes
Interleukin-15
Receptors, Interleukin-5
Interleukin-13
Interferon-gamma
Interleukin-3
Interleukin-11
Phytohemagglutinins
Interleukin-1beta
Signal Transduction
RNA, Messenger
Interleukin-12
Lymphokines
Enzyme-Linked Immunosorbent Assay
Interleukin-18
Biological Markers
Concanavalin A
Lipopolysaccharides
Lymphocyte Activation
Cell Division
Monocytes
B-Lymphocytes
Gene Expression Regulation
Granulocyte-Macrophage Colony-Stimulating Factor
Receptors, Interleukin-2
Macrophages
Growth Substances
Gene Expression
T-Lymphocytes, Helper-Inducer
Lymphocytes
Flow Cytometry
Cell Differentiation
Antigens, CD
Fibroblasts
Case-Control Studies
Reverse Transcriptase Polymerase Chain Reaction
Lung
Gene Expression Profiling
Dose-Response Relationship, Drug
Bone Marrow Cells
Molecular Sequence Data
Killer Cells, Natural
NF-kappa B
Oligonucleotide Array Sequence Analysis
Phenotype
Transfection
Base Sequence
Tumor Cells, Cultured
Prospective Studies
Polymerase Chain Reaction
Transcription, Genetic
Disease Models, Animal
Reciprocal control of T helper cell and dendritic cell differentiation. (1/3668)
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)Interaction of lipopolysaccharide with human small intestinal lamina propria fibroblasts favors neutrophil migration and peripheral blood mononuclear cell adhesion by the production of proinflammatory mediators and adhesion molecules. (2/3668)
Fibroblasts are important effector cells having a potential role in augmenting the inflammatory responses in various diseases. In infantile diarrhea caused by enteropathogenic Escherichia coli (EPEC), the mechanism of inflammatory reactions at the mucosal site remains unknown. Although the potential involvement of fibroblasts in the pathogenesis of cryptococcus-induced diarrhea in pigs has been suggested, the precise role of lamina propria fibroblasts in the cellular pathogenesis of intestinal infection and inflammation caused by EPEC requires elucidation. Earlier we reported the lipopolysaccharide (LPS)-induced cell proliferation, and collagen synthesis and downregulation of nitric oxide in lamina propria fibroblasts. In this report, we present the profile of cytokines and adhesion molecules in the cultured and characterized human small intestinal lamina propria fibroblasts in relation to neutrophil migration and adhesion in response to lipopolysaccharide (LPS) extracted from EPEC 055:B5. Upon interaction with LPS (1-10 micrograms/ml), lamina propria fibroblasts produced a high level of proinflammatory mediators, interleukin (IL)-1alpha, IL-1beta, IL-6, IL-8, tumor necrosis factor (TNF)-alpha and cell adhesion molecules (CAM) such as intercellular cell adhesion molecule (ICAM), A-CAM, N-CAM and vitronectin in a time-dependent manner. LPS induced cell-associated IL-1alpha and IL-1beta, and IL-6, IL-8 and TNF-alpha as soluble form in the supernatant. Apart from ICAM, vitronectin, A-CAM, and N-CAM proteins were strongly induced in lamina propria fibroblasts by LPS. Adhesion of PBMC to LPS-treated lamina propria fibroblasts was ICAM-dependent. LPS-induced ICAM expression in lamina propria fibroblasts was modulated by whole blood, PBMC and neutrophils. Conditioned medium of LPS-treated lamina propria fibroblasts remarkably enhanced the neutrophil migration. The migration of neutrophils was inhibited by anti-IL-8 antibody. Co-culture of fibroblasts with neutrophils using polycarbonate membrane filters exhibited time-dependent migration of neutrophils. These findings indicate that the coordinate production of proinflammatory cytokines and adhesion molecules in lamina propria fibroblasts which do not classically belong to the immune system can influence the local inflammatory reactions at the intestinal mucosal site during bacterial infections and can influence the immune cell population residing in the lamina propria. (+info)Th1 and Th2 cytokine mRNA profiles in childhood nephrotic syndrome: evidence for increased IL-13 mRNA expression in relapse. (3/3668)
Idiopathic nephrotic syndrome of childhood is thought to be associated with T lymphocyte dysfunction often triggered by viral infections, with the production of circulating factor(s) resulting in proteinuria. In view of the conflicting evidence of T cell activation and Th1 or Th2 pattern of cytokine synthesis in this disease, this study examined the mRNA expression of interleukin-2 (IL-2), interferon-gamma, IL-4, and IL-13 from CD4+ and CD8+ T cells in steroid-responsive nephrotic patients in relapse and remission. Fifty-five children with steroid-responsive nephrotic syndrome were included in this study, together with 34 normal controls and 24 patient controls with viral infections. RNA was isolated from purified CD4+ or CD8+ cells from peripheral blood and subjected to reverse transcription-PCR. Cytokine mRNA expression was measured semiquantitatively, and a cytokine index was derived from densitometric readings, with cyclophilin as the housekeeping gene. Both cross-sectional and paired data showed an increased CD4+ and CD8+ IL-13 mRNA expression in patients with nephrotic relapse as compared to remission, normal, and patient controls (P < 0.008). This was also associated with increased cytoplasmic IL-13 expression in phorbol myristate acetate/ionomycin-activated CD3+ cells (6.66+/-3.39%) from patients with nephrotic relapse compared to remission (2.59+/-1.35%) (P < 0.0001). However, there was no significant difference in CD4+ or CD8+ IL-2, interferon-gamma and IL-4 mRNA expression. IL-13 is an important T cell cytokine with anti-inflammatory and immunomodulatory functions on B cells and monocytes. It is conceivable that IL-13 may act on monocytes to produce vascular permeability factor(s) involved in the pathogenesis of proteinuria in patients with relapse nephrotic syndrome. (+info)Enhanced capacity of a widespread strain of Mycobacterium tuberculosis to grow in human macrophages. (4/3668)
To determine whether the extent of spread of Mycobacterium tuberculosis strains in the community correlated with their capacity to replicate in human macrophages, intracellular growth rates of M. tuberculosis patient isolates were measured. Strain 210 caused disease in 43 patients in central Los Angeles, 3 "small-cluster" strains caused disease in 8-23 patients, and 5 "unique" strains each caused disease in only 1 patient who was positive by sputum acid-fast smear and spent substantial amounts of time at homeless shelters that were tuberculosis transmission sites. Strain 210 isolates grew significantly more rapidly than small-cluster and unique strains in macrophages. All strains elicited production of similar amounts of tumor necrosis factor-alpha, interleukin (IL)-6, IL-10, and IL-12 and were equally susceptible to reactive nitrogen intermediates. It was concluded that the extensive spread of an M. tuberculosis strain correlated with its capacity to replicate rapidly in human macrophages, which may be a marker of virulence. (+info)Macrophages are a significant source of type 1 cytokines during mycobacterial infection. (5/3668)
T-helper 1 (Th1) cells are believed to be the major producer of the type 1 cytokine interferon-gamma (IFN-gamma) in cell-mediated immunity against intracellular infection. We have investigated the ability of macrophages to release type 1 cytokines and their regulatory mechanisms using both in vivo and in vitro models of pulmonary mycobacterial infection. During pulmonary infection by live Mycobacterium bovis bacilli Calmette-Guerin (BCG) in wild-type mice, lung macrophages released interleukin-12 (IL-12), IFN-gamma, and tumor necrosis factor-alpha (TNF-alpha), and expressed surface activation markers. However, macrophages in infected IL-12(-/-) mice released TNF-alpha but not IFN-gamma and lacked surface activation makers. In freshly isolated lung macrophages from naive IL-2(-/-) mice, mycobacteria alone released TNF-alpha but not IFN-gamma, whereas exogenously added IL-12 alone released a minimum of IFN-gamma. However, these macrophages released large quantities of IFN-gamma upon stimulation with both mycobacteria and IL-12. In contrast, mycobacteria and exogenous IFN-gamma released only a minimum of endogenous IFN-gamma. Endogenous IL-18 (IFN-gamma-inducing factor) played little role in IFN-gamma responses by macrophages stimulated by mycobacteria and IL-12. Our data reveal that macrophages are a significant source of type 1 cytokines during mycobacterial infection and that both IL-12 and intracellular pathogens are required for the release of IFN-gamma but not TNF-alpha. These findings suggest that macrophages regulate cell-mediated immunity by releasing not only IL-12 and TNF-alpha but also IFN-gamma and that full activation of IFN-gamma response in macrophages is tightly regulated. (+info)Regulation of TH1- and TH2-type cytokine expression and action in atopic asthmatic sensitized airway smooth muscle. (6/3668)
CD4(+) T helper (TH)1- and TH2-type cytokines reportedly play an important role in the pathobiology of asthma. Recent evidence suggests that proasthmatic changes in airway smooth muscle (ASM) responsiveness may be induced by the autocrine release of certain proinflammatory cytokines by the ASM itself. We examined whether TH1- and TH2-type cytokines are expressed by atopic asthmatic sensitized ASM and serve to autologously regulate the proasthmatic phenotype in the sensitized ASM. Expression of these cytokines and their receptors was examined in isolated rabbit and human ASM tissues and cultured cells passively sensitized with sera from atopic asthmatic patients or control subjects. Relative to controls, atopic sensitized ASM cells exhibited an early increased mRNA expression of the TH2-type cytokines, interleukin-5 (IL-5) and granulocyte-macrophage colony-stimulating factor (GM-CSF), and their receptors. This was later followed by enhanced mRNA expression of the TH1-type cytokines, IL-2, IL-12, and interferon-gamma (IFN-gamma), as well as their respective receptors. In experiments on isolated ASM tissue segments (a) exogenous administration of IL-2 and IFN-gamma to atopic asthmatic serum-sensitized ASM ablated both their enhanced constrictor responsiveness to acetylcholine (ACh) and their attenuated relaxation responsiveness to beta-adrenoceptor stimulation with isoproterenol, and (b) administration of IL-5 and GM-CSF to naive ASM induced significant increases in their contractility to ACh and impaired their relaxant responsiveness to isoproterenol. Collectively, these observations provide new evidence demonstrating that human ASM endogenously expresses both TH1- and TH2-type cytokines and their receptors, that these molecules are sequentially upregulated in the atopic asthmatic sensitized state, and that they act to downregulate and upregulate proasthmatic perturbations in ASM responsiveness, respectively. (+info)A fatal cytokine-induced systemic inflammatory response reveals a critical role for NK cells. (7/3668)
The mechanism of cytokine-induced shock remains poorly understood. The combination of IL-2 and IL-12 has synergistic antitumor activity in vivo, yet has been associated with significant toxicity. We examined the effects of IL-2 plus IL-12 in a murine model and found that the daily, simultaneous administration of IL-2 and IL-12 resulted in shock and 100% mortality within 4 to 12 days depending on the strain employed. Mice treated with IL-2 plus IL-12 exhibited NK cell apoptosis, pulmonary edema, degenerative lesions of the gastrointestinal tract, and elevated serum levels of proinflammatory cytokines and acute phase reactants. The actions of TNF-alpha, IFN-gamma, macrophage-inflammatory protein-1alpha, IL-1, IL-1-converting enzyme, Fas, perforin, inducible nitric oxide synthase, and STAT1 did not contribute to the observed toxicity, nor did B or T cells. However, toxicity and death from treatment with IL-2 plus IL-12 could be completely abrogated by elimination of NK cells. These results suggest that the fatal systemic inflammatory response induced by this cytokine treatment is critically dependent upon NK cells, but does not appear to be mediated by the known effector molecules of this cellular compartment. These data may provide insight into the pathogenesis of cytokine-induced shock in humans. (+info)Levels of IL-12 in the sera of patients with systemic lupus erythematosus (SLE)--relation to Th1- and Th2-derived cytokines. (8/3668)
IL-12 is a cytokine that induces Th1-derived cytokines (interferon-gamma (IFN-gamma) and IL-2). The significance of IL-12 in human autoimmunity is no clear, and the serum levels of IL-12 in SLE are not clearly established. Therefore, we examined the levels of IL-12 in 39 patients with active SLE, with sandwich ELISA. The levels of IL-12 in patients were significantly higher than in normal subjects. Patients with high levels of IL-12 also had high levels of IFN-gamma, while their levels of IL-13 were significantly lower than in patients with normal levels of IL-12. Patients with pulmonary involvement had high levels of IL-12, and steroid therapy decreased the IL-12 level in three patients. In a retrospective study of seven patients, various changes of IL-12 and IL-13 were recognized before disease flare. Thus, in SLE patients, the level of IL-12 was increased and this increase was related to the change of Th1- or Th2-derived cytokines with some organ involvement. (+info)There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
Interleukin
Interleukin 25
Interleukin 3
Interleukin 11
Interleukin 16
Interleukin 6
Interleukin-38
Interleukin 28
Interleukin 13
Interleukin 30
Interleukin 19
Interleukin 24
Interleukin 9
Interleukin 29
Interleukin 37
Interleukin 15
Interleukin 7
Interleukin 32
Interleukin 23
Interleukin 18
Interleukin 26
Interleukin 21
Interleukin 31
Interleukin 36
Interleukin 33
Interleukin 17F
Interleukin 22
Interleukin 5
Interleukin 27
Interleukin 34
DailyMed - Search Results for Interleukin-5 Antagonist
Deficiency of interleukin-18 in mice leads to hyperphagia, obesity and insulin resistance | Nature Medicine
Il1b MGI Mouse Gene Detail - MGI:96543 - interleukin 1 beta
WikiGenes - IL6 - interleukin 6
Browsing by Subject "Interleukin-11"
Interleukin 27 limits autoimmune encephalomyelitis by suppressing the development of interleukin 17-producing T cells
PRIME PubMed | Serum interleukin-18 in patients with chronic ordinary urticaria: association with disease activity
Recombinant Macaca mulatta Interleukin-10 (IL10) | CSB-YP011580MOW | Cusabio
Recombinant interleukin-2 directly augments the cytotoxicity of human monocytes. | Burnet Institute
Vesicular Palmoplantar Eczema Medication: Corticosteroids, Calcineurin Inhibitors, Retinoids, Retinoids, Immunosuppressants,...
Interleukin-11 Receptor Subunit Alpha-1 is Required for Maximal Airway Responsiveness to Methacholine After Acute Exposure to...
Interleukin-1 (IL-1) structural pathway (WP2637) - Homo sapiens | WikiPathways
Treatment of pancreatic cancer with an oncolytic adenovirus expressing interleukin-12 in Syrian hamsters
Interleukin-4 Gene Transfection and Spheroid Formation Potentiate Therapeutic Efficacy of Mesenchymal Stem Cells for...
Mesenchymal Stem Cells Inhibit the Differentiation of CD4+ T Cells into Interleukin-17-Secreting T Cells | Acta Haematologica |...
GMS | 60. Jahrestagung der Deutschen Gesellschaft für Neuropathologie und Neuroanatomie (DGNN) | Interleukin-10 receptor...
Cardiac death in a patient with adult-onset Still's disease treated with the interleukin 1 receptor inhibitor anakinra | Annals...
JCI Insight -
Interleukin-1 signaling contributes to acute islet compensation
WHO EMRO | Interleukins 12 and 13 levels among beta-thalassaemia major patients | Volume 19, issue 2 | EMHJ volume 19, 2013
The release of interleukin-26 from alveolar type II cells and its response to stimuli from Gram-negative and Gram-positive...
European Crohn´s and Colitis Organisation - ECCO - OP20 Perianal fistulas are characterised by expansion of interleukin-22...
Background To research whether monosodium urate (MSU) crystals induce interleukin (IL)-1 - Generation of a selective small...
Brain Extracellular Interleukin-6 Levels Decrease Following Antipyretic Therapy with Diclofenac in Patients with Spontaneous...
The prognostic value of interleukin-6 and D-dimer levels in primary HIV infection | HTB | HIV i-Base
Enzymes - Interleukin 11
Search Results - interleukin-12
Development and validation of a house finch interleukin-1β (HfIL-1β) ELISA system | BMC Veterinary Research | Full Text
Immune Cell Activation in Melioidosis: Increased Serum Levels of Interferon- and Soluble Interleukin-2 Receptors without...
Cytokine11
- Interleukin-17A (IL-17A) is the signature cytokine of the recently identified T helper 17 (Th17) cell subset. (nih.gov)
- Interleukin-18 binding protein: a novel modulator of the Th1 cytokine response. (nature.com)
- This cytokine is a ligand for interleukin 4 receptor. (nih.gov)
- The interleukin 4 receptor also binds to IL13, which may contribute to many overlapping functions of this cytokine and IL13. (nih.gov)
- Interleukin 13 ( IL-13 ) is a cytokine secreted by many cell types, but especially T helper type 2 (Th2) cells [1] , that is an important mediator of allergic inflammation and disease. (wikidoc.org)
- Interleukin-1, the first named Interleukin, is experiencing a true renaissance and many recent studies have uncovered yet new pivotal roles of this cytokine family in the regulation of inflammation and tissue homeostasis. (nih.gov)
- Interleukin (IL)-18 is a pleiotropic cytokine, which may play a role in autoimmune and allergic disorders. (unboundmedicine.com)
- AU - Tedeschi,A, AU - Lorini,M, AU - Suli,C, AU - Asero,R, Y1 - 2007/05/16/ PY - 2007/5/19/pubmed PY - 2008/2/26/medline PY - 2007/5/19/entrez SP - 568 EP - 70 JF - Clinical and experimental dermatology JO - Clin Exp Dermatol VL - 32 IS - 5 N2 - Interleukin (IL)-18 is a pleiotropic cytokine, which may play a role in autoimmune and allergic disorders. (unboundmedicine.com)
- Interleukin (IL)-6 is a pleiotropic, proinflammatory cytokine produced by a variety of cell types, including lymphocytes, monocytes, and fibroblasts. (nih.gov)
- Interleukin-21 is a T-helper cytokine that regulates humoral immunity and cell-mediated anti-tumour responses. (joplink.net)
- Interleukin (IL)- 37 is a newly discovered anti-inflammatory member of the IL-1 cytokine family and has been shown to be regulated in inflammatory disease. (nih.gov)
Serum1
- Elevated levels of interleukin-18 and tumor necrosis factor-alpha in serum of patients with type 2 diabetes mellitus: relationship with diabetic nephropathy. (nature.com)
Receptors6
- The interleukin-2 receptors: insights into a complex signalling mechanism. (nih.gov)
- Interleukin 2 and interleukin 2 receptors]. (nih.gov)
- Receptors, Interleukin-21" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
- Cell surface receptors for interleukin 21. (harvard.edu)
- This graph shows the total number of publications written about "Receptors, Interleukin-21" by people in Harvard Catalyst Profiles by year, and whether "Receptors, Interleukin-21" was a major or minor topic of these publication. (harvard.edu)
- Below are the most recent publications written about "Receptors, Interleukin-21" by people in Profiles. (harvard.edu)
Cytokines2
- In this context, cytokines of the interleukin (IL)-1 family play an important role in initiating inflammation and innate immunity, as well as in polarizing appropriate adaptive immune responses. (unige.ch)
- In the advanced stage of COVID-19, numerous inflammatory cytokines, such as interleukins (ILs), TNF and chemokines, are released and attack the immune organs and tissues ( 3-5 ). (spandidos-publications.com)
Signal Transduction1
- Possible mechanism for the alpha subunit of the interleukin-2 receptor (CD25) to influence interleukin-2 receptor signal transduction. (nih.gov)
Recombinant2
- In the present retrospective case‑control study, the potential therapeutic effect of recombinant human interleukin‑2 (rIL‑2) in patients with severe COVID‑19 was demonstrated. (spandidos-publications.com)
- Recombinant interleukin-2 directly augments the cytotoxicity of human monocytes. (edu.au)
Cytotoxicity2
- Anti-CD20-interleukin-21 fusokine targets malignant B cells via direct apoptosis and NK-cell-dependent cytotoxicity. (harvard.edu)
- Direct and immune-mediated cytotoxicity of interleukin-21 contributes to antitumor effects in mantle cell lymphoma. (harvard.edu)
Mice2
- The creation of mice with a specific defect in the interleukin-2 gene has given us a clearer idea of its role in vivo. (nih.gov)
- Neutralization of interleukin-18 reduces neutrophil tissue accumulation and protects mice against lethal Escherichia coli and Salmonella typhimurium endotoxemia. (nature.com)
Psoriasis2
- This drug is an interleukin (IL-23) inhibitor that's very effective and works long-term to control the symptoms of psoriasis. (skintherapyletter.com)
- With the availability of tildrakizumab (Ilumya), an interleukin-23 (IL-23) inhibitor, dermatologists are very optimistic about the continued success of this biologic drug used to treat psoriasis patients. (skintherapyletter.com)
Gene1
- Several subtypes of interleukin-17 have been identified, each of which is a product of a unique gene. (curehunter.com)
Inflammation1
- The structural pathway of interleukin 1 (IL-1) initiated signaling reveals mechanisms of oncogenic mutations and SNPs in inflammation and cancer. (wikipathways.org)
Human3
- Mutation of Asp20 of human interleukin-2 reveals a dual role of the p55 alpha chain of the interleukin-2 receptor. (nih.gov)
- Hier sind Interleukin 17a ELISA Kits für eine Vielzahl von Species wie anti-Human Interleukin 17a, anti-Mouse Interleukin 17a, anti-Cow Interleukin 17a zu finden. (antikoerper-online.de)
- Caption: Researchers used artificial intelligence to map hundreds of new protein structures, including this 3D view of human interleukin-12 (blue) bound to its receptor (purple). (nih.gov)
Cells3
- Its role in the activation of T cells by antigen-presenting cells, the structure-activity relationships between interleukin-2 and its receptor and the subsequent signaling have all become clearer. (nih.gov)
- Interleukin-2 (IL-2), originally described as a growth factor required for sustained proliferation of T cells in vitro is a glycoprotein hormone of known structure which appears to be important for the generation of immune responses in vivo. (edu.au)
- In this study production levels of interleukins (IL)-12 and IL-13 were measured by commercial ELISA in culture supernatants of mitogen-stimulated peripheral blood mononuclear cells from 30 non-splenectomized beta-thalassaemia cases with iron overload and 20 age- and sex-matched healthy individuals. (who.int)
Patients1
- Inhibition of interleukins 4 and 13 with dupilumab in patients with chronic rhinosinusitis with nasal polyps (CRSwNP) has shown to decrease polyp burden and improve symptoms. (medscape.com)
Therapy1
- Interleukin 21 - its potential role in the therapy of B-cell lymphomas. (harvard.edu)
Expression1
- Increased expression of interleukin-1 receptor type 1 in active endometriotic lesions. (wikipathways.org)
Levels1
- Research has shown high levels of effectiveness are maintained for 5 years and beyond with tildrakizumab (Ilumya), an interleukin-23 (IL-23) inhibitor. (skintherapyletter.com)
Role3
Family1
- This Symposium is offering presentations on new emerging aspects of the Interleukin-1 family biology by extramural and intramural investigators, some of which have been among the pioneers of this field of research. (nih.gov)
Central1
- Interleukin-13: central mediator of allergic asthma. (wikidoc.org)
Study1
- The Foundation is pleased to announce its partnership with Provention Bio to provide clinical trial recruitment for its Phase 2b PROACTIVE Celiac Study for PRV-015 (an anti-interleukin-15 monoclonal antibody). (celiac.org)
Cell1
- The team identified T-cell growth factor (TCFG), now known as interleukin-2 (IL-2). (nih.gov)
Method1
- Disclosed a sandwich method and a kit for assaying interleukin-2 receptor (IL-2R) in a sample. (nih.gov)
Receptor2
- Recently, several of the interleukin receptor antagonists have been assessed as therapy of the advanced hyperinflammatory state of severe COVID-19. (nih.gov)
- The interleukin receptor antagonists have been associated with rare instances of clinically apparent liver injury that is generally mild and resolves with discontinuation. (nih.gov)
Therapies1
- A greater understanding of the immunology of asthma and of the role of interleukins has led to new targeted therapies. (medscape.com)
Asthma5
- This article provides an extensive review of the role of interleukins in asthma. (medscape.com)
- This is a complex area and there are many different interleukins that are involved in the immunology of asthma. (medscape.com)
- Nevertheless, animal models and in vitro work have shown that many different interleukins play an important role in asthma and that their modulation can alter airway inflammation, hyper-responsiveness and airway remodeling. (medscape.com)
- Interleukins involved in asthma clinical trials. (medscape.com)
- Title : Interleukin (IL)-33 Immunobiology in Asthma and Airway Inflammatory Diseases Personal Author(s) : Gaurav, Rohit;Poole, Jill A. (cdc.gov)
Beneficial1
- Carefully selecting patient groups that may respond to novel biologic agents is vital in identifying whether specific interleukin modulation is beneficial. (medscape.com)
Clinical1
- As discussed, we are yet to see the development of an interleukin-modulating agent that has successfully progressed to clinical use. (medscape.com)
Diseases2
ALPHA1
- ITHURTS- anti-interleukin-1.alpha. (nih.gov)
Treatment2
- Review Interleukin-1 antagonists in the treatment of autoinflammatory syndromes, including cryopyrin-associated periodic syndrome. (nih.gov)
- Adjunctive treatment with interleukin-2 (IL-2 [Proleukin S, Novartis Pharma GmbH, Nuremberg, Germany]) was administered subcutaneously (4.5 × 10 6 IU) on 3 occasions in September, October, and November 2008. (cdc.gov)
Production2
- In this study production levels of interleukins (IL)-12 and IL-13 were measured by commercial ELISA in culture supernatants of mitogen-stimulated peripheral blood mononuclear cells from 30 non-splenectomized beta-thalassaemia cases with iron overload and 20 age- and sex-matched healthy individuals. (who.int)
- Dans la présente étude, les taux de production des interleukines 12 et 13 (IL-12 et IL-13) ont été mesurés à l'aide de la méthode ELISA dans les surnageants de culture de cellules mononucléées de sang périphérique stimulées par des mitogènes chez 30 cas de bêta-thalassémie non splénectomisés présentant une surcharge martiale ainsi que chez 20 individus en bonne santé appariés pour l'âge et le sexe. (who.int)