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The underlying mechanism driving this immunosuppressive function of TNFR2 remains unclear. We show here that chronic exacerbated EAE in TNFR2 KO mice is associated with increased Th17\u2010cell responses and reduced numbers of Foxp3<jats:sup>+<\/jats:sup> Treg cells both in the spinal cord and peripheral lymphoid organs. Treg cells from TNFR2\u2010deficient animals developing EAE show decreased proliferative and suppressive functions, both ex vivo and in vivo, and appear responsible for the exacerbated non\u2010remitting disease, as evidenced by phenotypic rescue following adoptive transfer of Treg cells from WT but not TNFR2<jats:sup>\u2212\/\u2212<\/jats:sup> donors. Reciprocal BM transplantation experiments between WT and TNFR2\u2010deficient mice demonstrated that the capacity of TNFR2 to support Treg\u2010cell expansion and function during EAE is non\u2010intrinsic to Treg or other haematopoietic cells but requires expression of TNFR2 in radiation\u2010resistant cells of the host. These results reveal a previously unsuspected role for non\u2010haematopoietic TNFR2 in modulating Treg\u2010cell expansion and immune suppression during development of autoimmunity and suggest that a similar mechanism may affect chronicity and relapses characterizing human autoimmune disease, including MS.<\/jats:p>","DOI":"10.1002\/eji.201141659","type":"journal-article","created":{"date-parts":[[2011,11,22]],"date-time":"2011-11-22T11:24:52Z","timestamp":1321961092000},"page":"403-412","source":"Crossref","is-referenced-by-count":51,"title":["TNFR2 on non\u2010haematopoietic cells is required for Foxp3<sup>+<\/sup> Treg\u2010cell function and disease suppression in 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