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<StructureSection load='2nvh' size='340' side='right' caption='Human interleukin-1 β chain complex with sulfate, [[2nvh]]' scene=''> | |||
'''Interleukin''' (IL) is a cytokine which functions in the immune system | == Function == | ||
* IL-1 is a group of 11 cytokines which regulate immune and inflammatory response. See [[Interleukin-1 beta]].<br /> | '''Interleukin''' (IL) is a cytokine which functions in the immune system. IL families are denoted by numbers<ref>PMID:3277884</ref>.<br /> | ||
* IL-2 is a cytokine made by leukocytes. It is used in cancer therapy to boost the immune system.<br /> | * '''IL-1''' is a group of 11 cytokines which regulate immune and inflammatory response. See [[Interleukin-1 beta]].<br /> | ||
* 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.<br /> | * '''IL-2''' is a cytokine made by leukocytes. It is used in cancer therapy to boost the immune system.<br /> | ||
* IL-4 induces the differentiation of naive helper T cells (Th0) to Th2 cells.<br /> | * '''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.<br /> | ||
* IL-5 stimulates B cell growth and increases immunoglobulin secretion.<br /> | * '''IL-4''' induces the differentiation of naive helper T cells (Th0) to Th2 cells.<br /> | ||
* IL-6 is both a pro-inflammatory cytokine and anti-inflammatory myokine. | * '''IL-5''' stimulates B cell growth and increases immunoglobulin secretion.<br /> | ||
* IL-7 is a cytokine important for B and T cells development.<br /> | * '''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 [[Stepler sandbox STAT3|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-8 induces chemotaxis and phagocytosis.<br /> | * '''IL-7''' is a cytokine important for B and T cells development.<br /> | ||
* IL-10 see [[Interleukin-10]].<br /> | * '''IL-8''' induces chemotaxis and phagocytosis.<br /> | ||
* IL-12 induces the differentiation of naive helper T cells (Th0) to Th1 cells.<br /> | * '''IL-10''' see [[Interleukin-10]] and [[Inflammation & Rheumatoid Arthritis]].<br /> | ||
* IL-13 induces the differentiation of naive helper T cells (Th0) to Th2 cells.<br /> | * '''IL-11''' involved in the stimulation of megakaryocyte maturation.<br /> | ||
* IL-15 see [[Interleukin-15]].<br /> | * ''' IL-12''' induces the differentiation of naive helper T cells (Th0) to Th1 cells. See [[Interleukin-12]].<br /> | ||
* IL-16 acts as chemoattractant, modulator of T cell activity and inhibitor of HIV replication.<br /> | * '''IL-13''' induces the differentiation of naive helper T cells (Th0) to Th2 cells.<br /> | ||
* IL-17 recruits monocytes and neutrophils to the site of inflammation.<br /> | * '''IL-15''' see [[Interleukin-15]].<br /> | ||
* IL-18 induces cell-mediated immunity following infection by microbial lipopolysaccharides.<br /> | * '''IL-16''' acts as chemoattractant, modulator of T cell activity and inhibitor of HIV replication.<br /> | ||
* IL-19 induces activation of the signal transducer and activator of STAT3.<br /> | * '''IL-17''' recruits monocytes and neutrophils to the site of inflammation.<br /> | ||
* IL-21 has potent effect on natural killer cells.<br /> | * '''IL-18''' induces cell-mediated immunity following infection by microbial lipopolysaccharides.<br /> | ||
* IL-22 stimulates inflammatory responses like S100 and defensin.<br /> | * '''IL-19''' induces activation of the signal transducer and activator of STAT3.<br /> | ||
* IL-23 induces activation of the signal transducer and activator of STAT4.<br /> | * ''' IL-21''' has potent effect on natural killer cells.<br /> | ||
* IL-28 has a role in the immune defense against viruses.<br /> | * '''IL-22''' stimulates inflammatory responses like S100 and defensin.<br /> | ||
* IL-29 similar to IL-28.<br /> | * ''' IL-23''' induces activation of the signal transducer and activator of STAT4.<br /> | ||
* IL-33 induces helper T cells, mast cells, eosinophils and basophils to produce type 2 cytokines.<br /> | * ''' IL-24''' induces activation of the signal transducer and activator of STAT1 and STAT3.<br /> | ||
* IL-34 increases growth or survival of monocytes.<br /> | * '''IL-28''' has a role in the immune defense against viruses.<br /> | ||
* '''IL-29''' similar to IL-28.<br /> | |||
* '''IL-33''' induces helper T cells, mast cells, eosinophils and basophils to produce type 2 cytokines.<br /> | |||
* '''IL-34''' increases growth or survival of monocytes.<br /> | |||
* '''IL-36''' acts on naïve CD4+ T cells.<br /> | |||
* ''' IL-37''' has a role in inhibiting both innate and adaptive immune responses.<br /> | |||
See also [[Growth factors]] | |||
== Relevance == | |||
Uncontrolled activation of IL-1 is a component of of some inflammatory diseases including gout<ref>PMID:26656658</ref>.<br /> | |||
IL-8 is implicated in inflammatory lung diseases<ref>PMID:14720072</ref>.<br /> | |||
IL-10 is implicated in inflammatory bowel disease<ref>PMID:22890722</ref>.<br /> | |||
IL-10 is a potent anti-inflammatory agent<ref>PMID:22428854</ref>.<br /> | |||
IL-23 is implicated in Crohn's disease<ref>PMID:24481050</ref>.<br /> | |||
== Disease == | |||
IL deficiency results in autoimmune disease<ref>PMID:19494218</ref>. | |||
==3D structures of interleukin== | ==3D structures of interleukin== | ||
[[Interleukin 3D structures]] | |||
</StructureSection> | |||
== References == | |||
<references/> | |||
[[Category: Topic Page]] |
Latest revision as of 15:53, 4 May 2022
FunctionInterleukin (IL) is a cytokine which functions in the immune system. IL families are denoted by numbers[1].
See also Growth factors RelevanceUncontrolled activation of IL-1 is a component of of some inflammatory diseases including gout[2]. IL-8 is implicated in inflammatory lung diseases[3]. DiseaseIL deficiency results in autoimmune disease[7]. 3D structures of interleukin
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ReferencesReferences
- ↑ 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