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http://hdl.handle.net/2445/175717
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DC Field | Value | Language |
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dc.contributor.author | Wang, Ninghai | - |
dc.contributor.author | Yigit, Burcu | - |
dc.contributor.author | van der Poel, Cees E. | - |
dc.contributor.author | Cuenca, Marta | - |
dc.contributor.author | Carroll, Michael C. | - |
dc.contributor.author | Herzog, Roland W. | - |
dc.contributor.author | Engel Rocamora, Pablo | - |
dc.contributor.author | Terhorst, Cox | - |
dc.date.accessioned | 2021-03-24T16:35:29Z | - |
dc.date.available | 2021-03-24T16:35:29Z | - |
dc.date.issued | 2019-04-17 | - |
dc.identifier.issn | 1664-3224 | - |
dc.identifier.uri | http://hdl.handle.net/2445/175717 | - |
dc.description.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. | - |
dc.format.extent | 12 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Frontiers Media | - |
dc.relation.isformatof | Reproducció del document publicat a: https://doi.org/10.3389/fimmu.2019.00831 | - |
dc.relation.ispartof | Frontiers in Immunology, 2019, vol. 10 | - |
dc.relation.uri | https://doi.org/10.3389/fimmu.2019.00831 | - |
dc.rights | cc-by (c) Wang, Ninghai et al., 2019 | - |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es | - |
dc.source | Articles publicats en revistes (Biomedicina) | - |
dc.subject.classification | Homeòstasi | - |
dc.subject.classification | Cèl·lules B | - |
dc.subject.classification | Cèl·lules T | - |
dc.subject.classification | Antígens | - |
dc.subject.other | Homeostasis | - |
dc.subject.other | B cells | - |
dc.subject.other | T cells | - |
dc.subject.other | Antigens | - |
dc.title | The Checkpoint Regulator SLAMF3 Preferentially Prevents Expansion of Auto-Reactive B Cells Generated by Graft-vs.-Host Disease | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.identifier.idgrec | 696498 | - |
dc.date.updated | 2021-03-24T16:35:29Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.pmid | 31057553 | - |
Appears in Collections: | Articles publicats en revistes (Biomedicina) |
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696498.pdf | 13.38 MB | Adobe PDF | View/Open |
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