Wang, NinghaiKeszei, MartonHalibozek, Peter J.Yigit, BurcuEngel Rocamora, PabloTerhorst, Cox2019-02-082019-02-082016-121521-6616https://hdl.handle.net/2445/128081The nine SLAM family (Slamf) receptors are positive or negative regulators of adaptive and innate immune responses, and of several autoimmune diseases. Here we report that the transfer of Slamf6-/- B6 CD4+ T cells into co-isogenic bm12 mice causes SLE-like autoimmunity with elevated levels of autoantibodies. In addition, significantly higher percentages of Tfh cells and IFN-γ-producing CD4+ cells, as well as GC B cells were observed. Interestingly, the expression of the Slamf6-H1 isoform in Slamf6-/- CD4+ T cells did not induce this lupus-like phenotype. By contrast, Slamf1-/- or Slamf5-/- CD4+ T cells caused the same pathology as WT CD4+ T cells. As the transfer of Slamf [1+6]-/- or Slamf [1+5+6]-/- CD4+ T cells induced WT levels of autoantibodies, the presence of Slamf1 was requisite for the induction of increased levels of autoantibodies by Slamf6-/- CD4+ T cells. We conclude that Slamf6 functions as an inhibitory receptor that controls autoimmune responses.8 p.application/pdfengcc-by-nc-nd (c) Elsevier B.V., 2016http://creativecommons.org/licenses/by-nc-nd/3.0/esMalalties autoimmunitàriesCèl·lules TAutoimmune diseasesT cellsinfo:eu-repo/semantics/article6676342019-02-08info:eu-repo/semantics/openAccess27368806