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Title: | The Checkpoint Regulator SLAMF3 Preferentially Prevents Expansion of Auto-Reactive B Cells Generated by Graft-vs.-Host Disease |
Author: | Wang, Ninghai Yigit, Burcu van der Poel, Cees E. Cuenca, Marta Carroll, Michael C. Herzog, Roland W. Engel Rocamora, Pablo Terhorst, Cox |
Keywords: | Homeòstasi Cèl·lules B Cèl·lules T Antígens Homeostasis B cells T cells Antigens |
Issue Date: | 17-Apr-2019 |
Publisher: | Frontiers Media |
Abstract: | Absence 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. |
Note: | Reproducció del document publicat a: https://doi.org/10.3389/fimmu.2019.00831 |
It is part of: | Frontiers in Immunology, 2019, vol. 10 |
URI: | http://hdl.handle.net/2445/175717 |
Related resource: | https://doi.org/10.3389/fimmu.2019.00831 |
ISSN: | 1664-3224 |
Appears in Collections: | Articles publicats en revistes (Biomedicina) |
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