Interleukin-25 , inflammatory response

Bhattacherjee, P. and Henderson, B. (1987). Inflammatory responses to intraocularly injected interleukin 1. Curr. Eye Res. 6, 929-934. 

The inflammatory response in UC is propagated by atypical type 2 helper T cells that produce proinflammatory cytokines such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor (TNF).7 As discussed previously, a genetic predisposition to UC may partially explain the development of excessive colonic and rectal inflammation. The finding of positive perinuclear antineutrophil cytoplasmic antibodies (pANCA) in association with the human leukocyte antigen (HLA)-DR2 allele in a large percentage of patients with UC supports this theory.4,12... 

Oxidized LDL provokes an inflammatory response mediated by a number of chemoattractants and cytokines (e.g., monocyte colony-stimulating factor, intercellular adhesion molecule, platelet-derived growth factor, transforming growth factors, interleukin-1, interleukin-6). 

Berg DJ, Leach MW, Kuhn R, Rajewsky K, Muller W, Davidson NJ, Rennick D Interleukin-10 but not interleukin-4 is a natural suppressant of cutaneous inflammatory responses. J Exp Med 1995 182 99-108. 

Mechanism of Action An interleukin-1 (IL-1) receptor antagonistthatblocksthebind-ing of IL 1, a protein that is a major mediator of joint disease and is present in excess amounts inpatients with rheumatoid arthritis. Therapeutic Effect Inhibits the inflammatory response. 

BOX 4.4. REDUCTION OF A DOMAIN THAT CONTRIBUTES TO AN ADVERSE (INFLAMMATORY) RESPONSE OF THE CYTOKINE INTERLEUKIN-1 P (IL-ip)... 

The two types of cell-mediated immunity involve basically different types of T cells. In the delayed-type hypersensitivity response, the T cell, TD, that reacts specifically with antigens secretes interleukins (see Box S3A) that attract and activate macrophages or other leukocytes, thereby causing a slowly developing inflammatory response. A second type of T cell, known as the T killer cell, TK, reacts specifically with antigen that is bound to target cells, causing their lysis. 

Murray PJ. 2006. Understanding and exploiting the endogenous interleukin 10/STAT3-mediated anti-inflammatory response. Curr Opin Pharmacol. 6 379-386. 

Witowski J., Ksiazek K., and Jorres A. (2004). Interleukin-17 a mediator of inflammatory responses. Cell Mol. Life Sci. 61 567-579. 

Penkowa M., Molinero A., Carrasco J., and Flidalgo J. (2001). Interleukin-6 deficiency reduces the brain inflammatory response and increases oxidative stress and neurodegeneration after kainic acid-induced seizures. Neuroscience 102 805-818. 

In addition to direct effects on genes regulating inflammation, glucocorticoids also inhibit the transcription factors that initiate synthesis of pro-inflammatory cytokines (e.g., interleukin-1, tumor necrosis factor), enzymes (e.g., COX-2, nitric oxide synthase), and receptor proteins (e.g., natural killer receptors).17,87,89 Glucocorticoids may also exert some of their effects via a membrane-bound receptor that regulates activity of macrophages, eosinophils, T lymphocytes, and several other types of cells involved in the inflammatory response.89 Consequently, glucocorticoids affect many aspects of inflammation, and their powerful anti-inflammatory effects in rheumatoid arthritis result from their ability to blunt various cellular and chemical components of the inflammatory response. 

Cytokine The general term used to describe proteins produced by various immune and inflammatory cells. These proteins act as intercellular chemical signals that help orchestrate immune and inflammatory responses. Common cytokines include the interferons, interleukins, and certain growth factors. 

Cytokines are a heterogenous group of polypeptide mediators that have been associated with activation of numerous functions, including the immune system and inflammatory responses. The cytokine families include, but are not limited to, interleukins, chemokines, tumor necrosis factors, interferons (INF-a, -0, and -y), colony-stimulating factors, growth factors, neuropoietins, and neurotrophins (see Table 13.4). 

Dello Russo C, Boulleme AI, Gavrilyuk V, Feinstein DL (2004) Inhibition of microglial inflammatory responses by norepinephrine effects on nitric oxide and interleukin-lbeta production../, Neuroinflammation 1 9. 

Takenaka et al., 2004), this protein has also been reported to induce interleukin-6 production by macrophages via a TLR2-independent mechanism (Gobert et al., 2004). Recognition of H. pylori peptidoglycan-derived muropeptides by the intracellular pattern recognition molecule Nodi can occur (Viala et al., 2004) and contribute to the development of the subsequent inflammatory response. 

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