ReceptorsintheTNFreceptorfamilyareassociatedwiththeinductionofapoptosis,aswellasinflammatorysignaling.TheFasreceptor(CD95)mediatesapoptoticsignalingbyFas-ligandexpressedonthesurfaceofothercells.TheFas-FasLinteractionplaysanimportantroleintheimmunesystemandlackofthissystemleadstoautoimmunity,indicatingthatFas-mediatedapoptosisremovesself-reactivelymphocytes.Fassignalingisalsoinvolvedinimmunesurveillancetoremovetransformedcellsandvirusinfectedcells.BindingofFAStooligimerizedFasLonanothercellactivatesapoptoticsignalingthroughacytoplasmicdomaintermedthedeathdomainthatinteractswithsignalingadaptorsincludingFAF,FADDandDAXtoactivatethecaspaseproteolyticcascade.Caspase-8andcaspase-10arefirstactivated,tothencleaveandactivatedownstreamcaspases,andavarietyofcellularsubstratesthatleadtocelldeath.Caspasescleavenuclearlamins,causingthenucleustobreakdownandloseitsnormalstructureandanothercaspasesubstrateisDFF,inducingcleavageanddegradationofthegenome.Othercaspasesubstratesareinvolvedincytoskeletalstructure,cellcycleregulationandsignalingpathways.ActivationofJNKkinase,activationofJun,andproductionofceramidemayalsoplayrolesinFas-mediatedapoptosis.Activationoffas-mediatedapoptosisisopposedbyI-FLICEandFAP.Virusesandtumorsmayescapeimmunesurveillanceinpartthroughsuppressionoffas-mediatedapoptosisusingsimilarmechanisms.

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