Wang, NinghaiYigit, Burcuvan der Poel, Cees E.Cuenca, MartaCarroll, Michael C.Herzog, Roland W.Engel Rocamora, PabloTerhorst, Cox2021-03-242021-03-242019-04-171664-3224https://hdl.handle.net/2445/175717Absence of the mouse cell surface receptor SLAMF3 in SLAMF3-/- mice suggested that this receptor negatively regulates B cell homeostasis by modulating activation thresholds of B cell subsets. Here, we examine whether anti-SLAMF3 affects both B and T cell subsets during immune responses to haptenated ovalbumin [NP-OVA] and in the setting of chronic graft vs. host disease (cGVHD) induced by transferring B6.C-H2 bm12/KhEg (bm12) CD4+ T cells into B6 WT mice. We find that administering αSLAMF3 to NP-OVA immunized B6 mice primarily impairs antibody responses and Germinal center B cell [GC B] numbers, whilst CXCR5+, PD-1+, and ICOS+ T follicular helper (TFH) cells are not significantly affected. By contrast, administering αSLAMF3 markedly enhanced autoantibody production upon induction of cGVHD by the transfer of bm12 CD4+ T cells into B6 recipients. Surprisingly, αSLAMF3 accelerated both the differentiation of GC B and donor-derived TFH cells initiated by cGVHD. The latter appeared to be induced by decreased numbers of donor-derived Treg and T follicular regulatory (TFR) cells. Collectively, these data show that control of anti-SLAMF3-induced signaling is requisite to prevent autoantibody responses during cGVHD, but reduces responses to foreign antigens.12 p.application/pdfengcc-by (c) Wang, Ninghai et al., 2019http://creativecommons.org/licenses/by/3.0/esHomeòstasiCèl·lules BCèl·lules TAntígensHomeostasisB cellsT cellsAntigensinfo:eu-repo/semantics/article6964982021-03-24info:eu-repo/semantics/openAccess31057553