The role of inflammasome‐derived IL‐1 in driving IL‐17 responses

Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society

关键词: Th17 cell;    γ;    δ;    T cell;    IL‐;    18;    caspase‐;    1;    autoimmunity;    infection;   

DOI  :  10.1189/jlb.1012543

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

NLRsaremembersofthePRRfamilythatsensemicrobialpathogensandmediatehostinnateimmuneresponsestoinfection.CertainNLRscanassembleintoamultiproteincomplexcalledtheinflammasome,whichactivatescasapse‐1requiredforthecleavageofimmatureformsofIL‐1βandIL‐18intoactive,maturecytokines.Theinflammasomeisactivatedbyconserved,exogenousmoleculesfrommicrobesandnonmicrobialmolecules,suchasasbestos,alum,orsilica,aswellasbyendogenousdangersignals,suchasATP,amyloid‐β,andsodiumuratecrystals.ActivationoftheinflammasomeisacriticaleventtriggeringIL‐1‐driveninflammationandiscentraltothepathologyofautoinflammatorydiseases,suchasgoutandMWS.RecentstudieshavealsoshownIL‐1orIL‐18,insynergywithIL‐23,canpromoteIL‐17‐prductionfromTh17cellsandγδTcells,andthisprocesscanberegulatedbyautophagy.IL‐1‐drivenIL‐17productionplaysacriticalroleinhostprotectiveimmunitytoinfectionwithfungi,bacteria,andcertainviruses.However,Th17cellsandIL‐17‐secetingγδTcells,activatedbyinflammasome‐derivedIL‐1orIL‐18,havemajorpathogenicrolesinmanyautoimmunediseases.Consequently,inflammasomesarenowmajordrugtargetsformanyautoimmuneandchronicinflammatorydiseases,aswellasautoinflammatorydiseases...

【 授权许可】

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