RegulationofTcellactivationisacrucialcomponentofbalancedfunctioningoftheimmunesystem.IftheTcellresponseistoogreatandactivationofself-responsivecellsorunstimulatedcellsisnotsuppressed,thenautoimmunedisordersortissueinjurycanresult.UnstimulatedTcellsaremaintainedinaquiescentstateandtheactivityofself-reactiveTcellsismaintainedinananergicstateinwhichIL-2expressionisrepressed.IL-2isacytokinewithakeyroleintheactivationandproliferationofTcells.ThemaintenanceofTcellsintheanergicorunstimulatedstatemaynotinvolvejustanabsenceofactivation,butanactiverepressionofIL-2expression,Tcellproliferationandactivation.TGFbetamayplayaroleinsuppressingTcellactivation.TobisafactoridentifiedrecentlythatrepressesTcellactivationthatisamemberofafamilyofgeneswithanti-proliferativeproperties.TobexpressionishighestinunstimulatedandanergicTcells,andisreducedinactivatedTcells.TobinteractswiththeTGFactivatedtranscriptionfactorsSMAD2andSMAD4,increasingtheirbindingtotheIL-2promoter,andhelpingtorepressIL-2expression.ThisroleofTobsuggeststhatinterferenceinTob’sfunctionmayleadtoautoimmunedisease.

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REFERENCES:TzachanisD,FreemanGJ,HiranoN,vanPuijenbroekAA,DelfsMW,BerezovskayaA,NadlerLM,BoussiotisVA.TobisanegativeregulatorofactivationthatisexpressedinanergicandquiescentTcells.NatImmunol.2001Dec;2(12):1174-82.Tzachanis,D.,Lafuente,E.,andBoussiotis,V.,A.TOBisanegativeregulatoroft-cellactivationandcytokinetranscription.Mod.Asp.Immunobiol.2(3),117-120,2002

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