期刊
SCIENTIFIC REPORTS
卷 8, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-018-19965-z
关键词
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资金
- British Heart Foundation (BHF)
- Medical Research Council (MRC) Centre for Transplantation, King's College London, UK-MRC grant [MR/J006742/1]
- Deanship of Scientific Research (DSR) at King Abdulaziz University, Jeddah [G-438-290-37]
- DSR
- National Institute for Health Research (NIHR) Biomedical Research Centre based at Guy's and Sthomas' NHS Foundation Trust and King's College London
- British Heart Foundation [PG/11/7/28621, RG/13/12/30395, RG/08/005/25303] Funding Source: researchfish
- Medical Research Council [MR/L022699/1, MR/J006742/1, MC_PC_14105] Funding Source: researchfish
- MRC [MR/L022699/1, MC_PC_14105] Funding Source: UKRI
Galectin-1 (Gal-1) is required for the development of B cells in the bone marrow (BM), however very little is known about the contribution of Gal-1 to the development of B cell regulatory function. Here, we report an important role for Gal-1 in the induction of B cells regulatory function. Mice deficient of Gal-1 (Gal-1(-/-)) showed significant loss of Transitional-2 (T2) B cells, previously reported to include IL-10(+) regulatory B cells. Gal-1(-/-)B cells stimulated in vitro via CD40 molecules have impaired IL-10 and Tim-1 expression, the latter reported to be required for IL-10 production in regulatory B cells, and increased TNF-alpha expression compared to wild type (WT) B cells. Unlike their WT counterparts, T2 and T1 Gal-1(-/-) B cells did not suppress TNF-a expression by CD4(+) T cells activated in vitro with allogenic DCs (allo-DCs), nor were they suppressive in vivo, being unable to delay MHC-class I mismatched skin allograft rejection following adoptive transfer. Moreover, T cells stimulated with allo-DCs show an increase in their survival when co-cultured with Gal-1(-/-)T2 and MZ B cells compared to WT T2 and MZ B cells. Collectively, these data suggest that Gal-1 contributes to the induction of B cells regulatory function.
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