The Journal of Experimental Medicine
1–2 wk.Nevertheless,themechanismof immunodeficient recipientswherediabetesdevelopswithin when CD4Tcellsfromdiabeticmicearetransferredinto transgenic models(3,5,6),thediseasecanbeprecipitated Introduction it wasnotobviouswhetherthelatephaseof NOD miceexhibitedadelayedonsetofdisease(7,8),but has remainedobscure.Itbecameclearthatperforin-deficient [email protected] (617) 632-6882;Fax:632-6881; e-mail: Dana-Farber CancerInstitute,44Binney St.,Boston,MA02115,Phone: Address correspondencetoHaraldvon Boehmer,HarvardMedicalSchool, destruction of cells causepancreaticisletcellinfiltrationwithsubsequent CD4 orCD8Tcellsspecificforantigensexpressedin been developedinwhichparticularlyhighfrequenciesof T cellreceptortransgenicmodelsoftype1diabeteshave (g7) MHCallelethatcontrolsdisease.Inaddition,several T cellsbypeptidespresentedtheparticularNODclassII model, thediseasedependsonactivationofautoimmune suitable animalmodelofhumantype1diabetes(1,2).Inthis Nonobese diabetic(NOD)micearethoughttorepresenta Fas waspresenton develop diabetes(9).Additionalanalyseshadsuggestedthat deficient lpr/lprmiceontheNODbackgrounddidnot was affected.Ontheotherhand,itshownthatFas-