Interleukin-6, role

Interleukin-1 OC and (3. IL-1 has radioprotective activity toward BM and other tissues (151,164). IL-1 is produced in response to endotoxin, other cytokines, and microbial and viral agents, primarily by monocytes and macrophages. Other nucleated cells can also produce it. IL-1 appears to play an important role in the regulation of normal hemopoiesis directly by stimulating the most primitive stem cells and indirectly by stimulating other hemopoietic factors, including G-CSF, GM-CSF, M-CSF, and IL-6. 

The interleukin-1 (EL-1) family of proteins currently comprises IL-1 a, IL-1 (3, and the IL-1 receptor antagonist (IL-1RA). The biological activities of EL-1 are shared by IL-1 a and IL-1 (3, whereas IL-1RA is a true receptor antagonist. IL-1 is a key player in acute and chronic inflammatory diseases. Whether IL-1 has a role in normal physiology is still unresolved. IL-1 can... 

In conclusion, IFNs have proven to be invaluable tools in the fight against chronic viral hepatitis. In these indications, their antiviral properties play a major role and it remains unclear whether their immunomodulatory properties are also important. Disappointing results obtained with purely immunomodulatory molecules, such as interleukins or Toll-like receptor agonists suggest that, if immunomodulation plays any role, potent inhibition of viral replication is also needed. The role of IFNs in the treatment of viral infections other than hepatitis B and C remains elusive. 

Dumoutier L, Tounsi A, Michiels T, Sommereyns C, Kotenko SV, Renauld JC (2004) Role of the interleukin (lL)-28 receptor tyrosine residues for antiviral and antiproliferative activity of lL-29/interferon-lambda 1 similarities with type I interferon signaling. J Biol Chem 279 ... 

K Role of interleukin-10 in specific immunotherapy. J Clin Invest 1998 102 98-106. 

These proteins are called acute phase proteins (or reactants) and include C-reactive protein (CRP, so-named because it reacts with the C polysaccharide of pneumococci), ai-antitrypsin, haptoglobin, aj-acid glycoprotein, and fibrinogen. The elevations of the levels of these proteins vary from as little as 50% to as much as 1000-fold in the case of CRP. Their levels are also usually elevated during chronic inflammatory states and in patients with cancer. These proteins are believed to play a role in the body s response to inflammation. For example, C-reactive protein can stimulate the classic complement pathway, and ai-antitrypsin can neutralize certain proteases released during the acute inflammatory state. CRP is used as a marker of tissue injury, infection, and inflammation, and there is considerable interest in its use as a predictor of certain types of cardiovascular conditions secondary to atherosclerosis. Interleukin-1 (IL-1), a polypeptide released from mononuclear phagocytic cells, is the principal—but not the sole—stimulator of the synthesis of the majority of acute phase reactants by hepatocytes. Additional molecules such as IL-6 are involved, and they as well as IL-1 appear to work at the level of gene transcription. 

Interleukin-2-inducible T cell kinase (ITK) is expressed mainly in T-lymphocytes and plays a major role in the activation of T-cells. Thus inhibitors of ITK should be useful as immunosuppressives and antiinflammatory agents. Snow et al. [67] describe a novel series of 2-aminobenzimidazole ITK inhibitors which is optimized... 

Inflammatory cytokines have been implicated in the pathophysiology of HF.9 Several proinflammatory (e.g., tumor necrosis factor-a [TNF-a], interleukin-1, interleukin-6, and interferon-y) and anti-inflammatory cytokines (e.g., interleukin-10) are overexpressed in the failing heart. The most is known about TNF-a, a pleiotrophic cytokine that acts as a negative inotrope, stimulates cardiac cell apoptosis, uncouples 3-adrenergic receptors from adenylyl cyclase, and is related to cardiac cachexia. The exact role of cytokines and inflammation in HF pathophysiology continues to be studied. 

Activated T cells begin releasing cytokines including interleukin-2 (IL-2), interferon-y, (IFN-y), tumor necrosis factor (TNF-a), and others.4,13 Cytokine activity leads to a rapid proliferation and turnover of skin cells, triggering the inflammatory process and the development of psoriatic skin lesions.4,13,14 TNF-a may have a role in disease severity it upregulates endothelial and keratinocyte expression of ICAM-1,... 

Multiple factors play a role in the development of AOM. Viral infection of the nasopharynx impairs eustachian tube function and causes mucosal inflammation, impairing mucociliary clearance and promoting bacterial proliferation and infection. Children are predisposed to AOM because their eustachian tubes are shorter, more flaccid, and more horizontal than adults, which make them less functional for drainage and protection of the middle ear from bacterial entry. Clinical signs and symptoms of AOM are the result of host immune response and damage to cells caused by inflammatory mediators such as tumor necrosis factor and interleukins that are released from bacteria.4... 

Clark-Lewis I, Schumacher C, Baggiofini M, Moser B. Structure-activity relationships of interleukin-8 determined using chemically synthesized analogs. Critical role of NH2-terminal residues and evidence for uncoupling of neutrophil chemo-taxis, exocytosis, and receptor binding activities. J Biol Chem 1991 266 23128-34. 

Fibbe WE, Pruijt JF, van Kooyk Y, Figdor CG, Opdenakker G, Willemze R. The role of metalloproteinases and adhesion molecules in interleukin-8-induced stemcell mobilization. Semin Hematol 2000 37(1 Suppl 2) 19-24. 

Szekanecz Z, Shah MR, Harlow LA, Pearce WH, Koch AE. Interleukin-8 and tumor necrosis factor-alpha are involved in human aortic endothelial cell migration. The possible role of these cytokines in human aortic aneurysmal blood vessel growth. Pathobiology 1994 62(3) 134-139. 

Flood-Page PT, Menzies-Gow AN, Kay AB, Robinson DS. EosinophiTs role remains uncertain as anti-interleukin-5 only partially depletes numbers in asthmatic airway. Am J Respir Crit Care Med 2003 167(2) 199-204. 

Pease JE, Sabroe I. The role of interleukin-8 and its receptors in inflammatory lung disease implications for therapy. Am J Respir Med 2002 1(1) 19-25. 

Varney ML, Li A, Dave BJ, Bucana CD, Johansson SL, Singh RK. Expression of CXCR1 and CXCR2 receptors in malignant melanoma with different metastatic potential and their role in interleukin-8 (CXCL-8)-mediated modulation of metastatic phenotype. Clin Exp Metastasis 2003 20 723-731. 

D20. Dinarello, C. A., Aiura, K., and Gelfland, J. A., The role of interleukin-1 in septic shock. In Yearbook of Intensive Care and Emergency Medicine (J.-L. Vincent, ed.) Springer-Verlag, Berlin, 25-35 (1992). 

Z8. Zuckerman, S. H., Shellhaas, J., and Butler, L. D., Differential regulation of lipopolysaccharide-induced interleukin I and tumor necrosis factor synthesis Effects of endogenous and exogenous glucocorticoids and the role of the pituitary-adrenal axis. Eur. J. Immunol. 19,301-305 (1989). 

McKenzie, G.J., Bancroft, A.J., Grencis, R.K. and McKenzie, A.N.J. (1998b) A distinct role for interleukin-13 in Th2-cell-mediated immune responses. Current Biology 8, 339-342. 

Mizoguchi, A., Mizoguchi, E. and Bhan, A.K. (1999) The critical role of interleukin 4 but not interferon gamma in the pathogenesis of colitis in T-cell receptor alpha mutant mice. Gastroenterology 116, 320-326. 

Given the role of H. pylori infection in gastric cancer and duodenal ulcer disease, one must note that certain interleukin-1 gene cluster polymorphisms (suspected of increasing production of interleukin-1-/1) are associated with a predisposition to hypochlorhydria and gastric cancer [52]. One of these host DNA polymorphisms involves a TATA box. 

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