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{{STRUCTURE_2nvh|  PDB=2nvh | SIZE=300| SCENE= |right|  CAPTION=Human interleukin-1 β chain complex with sulfate, [[2nvh]] }}
<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.  IL deficiency results in autoimmune disease.  IL families are denoted by numbers.  For some detailed interleukins see [[Interleukin-10]] and [[Interleukin-15]].
== Function ==
'''Interleukin''' (IL) is a cytokine which functions in the immune system.  IL families are denoted by numbers<ref>PMID:3277884</ref>.<br />
* '''IL-1''' is a group of 11 cytokines which regulate immune and inflammatory responseSee [[Interleukin-1 beta]].<br />
* '''IL-2''' is a cytokine made by leukocytes.  It is used in cancer therapy to boost the immune system.<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-4''' induces the differentiation of naive helper T cells (Th0) to Th2 cells.<br />
* '''IL-5''' stimulates B cell growth and increases immunoglobulin secretion.<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-7''' is a cytokine important for B and T cells development.<br />
* '''IL-8''' induces chemotaxis and phagocytosis.<br />
* '''IL-10''' see [[Interleukin-10]] and [[Inflammation & Rheumatoid Arthritis]].<br />
* '''IL-11''' involved in the stimulation of megakaryocyte maturation.<br />
* ''' IL-12''' induces the differentiation of naive helper T cells (Th0) to Th1 cells.  See [[Interleukin-12]].<br />
* '''IL-13''' induces the differentiation of naive helper T cells (Th0) to Th2 cells.<br />
* '''IL-15''' see [[Interleukin-15]].<br />
* '''IL-16''' acts as chemoattractant, modulator of T cell activity and inhibitor of HIV replication.<br />
* '''IL-17''' recruits monocytes and neutrophils to the site of inflammation.<br />
* '''IL-18''' induces cell-mediated immunity following infection by microbial lipopolysaccharides.<br />
* '''IL-19''' induces activation of the signal transducer and activator of STAT3.<br />
* ''' IL-21''' has potent effect on natural killer cells.<br />
* '''IL-22''' stimulates inflammatory responses like S100 and defensin.<br />
* ''' IL-23''' induces activation of the signal transducer and activator of STAT4.<br />
* ''' IL-24''' induces activation of the signal transducer and activator of STAT1 and STAT3.<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 />


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== Disease ==
IL deficiency results in autoimmune disease<ref>PMID:19494218</ref>.
==3D structures of factor IX==


==3D structures of interleukin==
[[Interleukin 3D structures]]


  [[Category:Topic Page]]
</StructureSection>
 
== References ==
<references/>
[[Category: Topic Page]]

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Michal Harel, Joel L. Sussman, Alexander Berchansky