Interleukin

From Proteopedia

1 Function
2 Relevance
3 Disease
4 3D structures of interleukin

Function

Interleukin (IL) is a cytokine which functions in the immune system. IL families are denoted by numbers^[1].

IL-1 is a group of 11 cytokines which regulate immune and inflammatory response. See Interleukin-1 beta.
IL-2 is a cytokine made by leukocytes. It is used in cancer therapy to boost the immune system.
IL-3 improves the body's natural response to disease by stimulating the differentiation of multipotent hematopoietic stem cells into myeloid or lymphoid progenitor cells.
IL-4 induces the differentiation of naive helper T cells (Th0) to Th2 cells.
IL-5 stimulates B cell growth and increases immunoglobulin secretion.
IL-6 is both a pro-inflammatory cytokine and anti-inflammatory myokine. Several studies have outlined the importance of autocrine IL-6 signaling in lung and breast cancers. For example, one group found a positive correlation between persistently activated tyrosine-phosphorylated STAT3 (pSTAT3), found in 50% of lung adenocarcinomas, and IL-6. Further investigation revealed that mutant EGFR could activate the oncogenic STAT3 pathway via upregulated IL-6 autocrine signaling.
IL-7 is a cytokine important for B and T cells development.
IL-8 induces chemotaxis and phagocytosis.
IL-10 see Interleukin-10 and Inflammation & Rheumatoid Arthritis.
IL-11 involved in the stimulation of megakaryocyte maturation.
IL-12 induces the differentiation of naive helper T cells (Th0) to Th1 cells. See Interleukin-12.
IL-13 induces the differentiation of naive helper T cells (Th0) to Th2 cells.
IL-15 see Interleukin-15.
IL-16 acts as chemoattractant, modulator of T cell activity and inhibitor of HIV replication.
IL-17 recruits monocytes and neutrophils to the site of inflammation.
IL-18 induces cell-mediated immunity following infection by microbial lipopolysaccharides.
IL-19 induces activation of the signal transducer and activator of STAT3.
IL-21 has potent effect on natural killer cells.
IL-22 stimulates inflammatory responses like S100 and defensin.
IL-23 induces activation of the signal transducer and activator of STAT4.
IL-24 induces activation of the signal transducer and activator of STAT1 and STAT3.
IL-28 has a role in the immune defense against viruses.
IL-29 similar to IL-28.
IL-33 induces helper T cells, mast cells, eosinophils and basophils to produce type 2 cytokines.
IL-34 increases growth or survival of monocytes.
IL-36 acts on naïve CD4+ T cells.
IL-37 has a role in inhibiting both innate and adaptive immune responses.

Relevance

Uncontrolled activation of IL-1 is a component of of some inflammatory diseases including gout^[2].
IL-8 is implicated in inflammatory lung diseases^[3].
IL-10 is implicated in inflammatory bowel disease^[4].
IL-10 is a potent anti-inflammatory agent^[5].
IL-23 is implicated in Crohn's disease^[6].

Disease

IL deficiency results in autoimmune disease^[7].

3D structures of interleukin

Interleukin 3D structures

References

↑ Dinarello CA. Biology of interleukin 1. FASEB J. 1988 Feb;2(2):108-15. PMID:3277884
↑ Schett G, Dayer JM, Manger B. Interleukin-1 function and role in rheumatic disease. Nat Rev Rheumatol. 2016 Jan;12(1):14-24. doi: 10.1038/nrrheum.2016.166. Epub 2015, Dec 10. PMID:26656658 doi:http://dx.doi.org/10.1038/nrrheum.2016.166
↑ 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. PMID:14720072
↑ Shah N, Kammermeier J, Elawad M, Glocker EO. Interleukin-10 and interleukin-10-receptor defects in inflammatory bowel disease. Curr Allergy Asthma Rep. 2012 Oct;12(5):373-9. doi: 10.1007/s11882-012-0286-z. PMID:22890722 doi:http://dx.doi.org/10.1007/s11882-012-0286-z
↑ Iyer SS, Cheng G. Role of interleukin 10 transcriptional regulation in inflammation and autoimmune disease. Crit Rev Immunol. 2012;32(1):23-63. PMID:22428854
↑ Eken A, Singh AK, Oukka M. Interleukin 23 in Crohn's disease. Inflamm Bowel Dis. 2014 Mar;20(3):587-95. doi:, 10.1097/01.MIB.0000442014.52661.20. PMID:24481050 doi:http://dx.doi.org/10.1097/01.MIB.0000442014.52661.20
↑ Aksentijevich I, Masters SL, Ferguson PJ, Dancey P, Frenkel J, van Royen-Kerkhoff A, Laxer R, Tedgard U, Cowen EW, Pham TH, Booty M, Estes JD, Sandler NG, Plass N, Stone DL, Turner ML, Hill S, Butman JA, Schneider R, Babyn P, El-Shanti HI, Pope E, Barron K, Bing X, Laurence A, Lee CC, Chapelle D, Clarke GI, Ohson K, Nicholson M, Gadina M, Yang B, Korman BD, Gregersen PK, van Hagen PM, Hak AE, Huizing M, Rahman P, Douek DC, Remmers EF, Kastner DL, Goldbach-Mansky R. An autoinflammatory disease with deficiency of the interleukin-1-receptor antagonist. N Engl J Med. 2009 Jun 4;360(23):2426-37. doi: 10.1056/NEJMoa0807865. PMID:19494218 doi:10.1056/NEJMoa0807865