c-Maf-dependentregulatoryTcellsmediateimmunologicaltolerancetoagutpathobiontMoXu1,*,MariaPokrovskii1,*,YiDing2,RenYi4,ChristyAu1,8,OliverJ.Harrison5,CarolinaGalan1,YasmineBelkaid5,6,RichardBonneau3,4,7,andDanR.Littman1,81MolecularPathogenesisProgram,TheKimmelCenterforBiologyandMedicineoftheSkirballInstitute,NewYorkUniversitySchoolofMedicine,NewYork,NY10016,USA2DepartmentofPathologyandLaboratoryMedicine,UniversityofRochesterMedicalCenter,Rochester,NY14642,USA3CenterforGenomicsandSystemsBiology,DepartmentofBiology,NewYorkUniversity,NewYork,NY10003,USA4CourantInstituteofMathematicalSciences,ComputerScienceDepartment,NewYorkUniversity,NewYork,NY10003,USA5MucosalImmunologySection,LaboratoryofParasiticDiseases,NationalInstituteofAllergyandInfectiousDiseases,NIH,Bethesda,MD20892,USA6NIAIDMicrobiomeProgram,NIH,Bethesda,MD20892,USA7CenterforComputationalBiology,FlatironInstitute,SimonsFoundation,NewYork,NY10010,USA8TheHowardHughesMedicalInstituteAbstractBothmicrobialandhostgeneticfactorscontributetothepathogenesisofautoimmunedisease1–4.Accumulatingevidencesuggeststhatmicrobialspeciesthatpotentiatechronicinflammation,asininflammatoryboweldisease(IBD),oftenalsocolonizehealthyindividuals.Thesemicrobes,includingtheHelicobacterspecies,havethepropensitytoinducepathogenicTcellsandarecollectivelyreferredtoaspathobionts4–6.However,anunderstandingofhowsuchTcellsareconstrainedinhealthyindividualsislacking.HerewereportthathosttolerancetoapotentiallyUsersmayview,print,copy,anddownloadtextanddata-minethecontentinsuchdocuments,forthepurposesofacademicresearch,subjectalwaystothefullConditionsofuse:http://www.nature.com/authors/editorial_policies/license.html#termsReprintsandpermissionsinformationisavailableatwww.nature.com/reprints.CorrespondenceandrequestsformaterialsshouldbeaddressedtoD.R.L.(Dan.Littman@med.nyu.edu).*Theseauthorscontributedequallytothiswork.SupplementaryInformationisavailableintheonlineversionofthepaper.AuthorContributionsM.X.andM.P.designedandperformedallexperiments...
