期刊
JOURNAL OF IMMUNOLOGY
卷 200, 期 8, 页码 2592-2602出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1701231
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资金
- National Institutes of Health [5T32HL007627, R37AI38310, R01AI46414, P01AI56299]
- National Multiple Sclerosis Society
- International Society for Advancement of Cytometry through a Marylou Ingram Scholar award
The programmed death (PD)-1 coinhibitory receptor regulates the balance between T cell activation and tolerance. Although the PD-1 ligands, PD-L1 and PD-L2, are expressed on a variety of cell types, the cell type-specific functions of PD-1 ligands in inducing signals through PD-1 are unknown. In this study, we use PD-L1 conditional knockout mice to investigate the cell type-specific functions of PD-L1. We demonstrate that PD-L1 expressed on dendritic cells (DCs), and to a lesser extent on B cells, attenuates the progression of experimental autoimmune encephalomyelitis and inhibits naive and effector T cells. PD-1 is highly expressed on effector populations, including T follicular helper (TFH) cells and T follicular regulatory (TFR) cells, which reside in germinal centers. We also show that DC PD-L1 is essential for limiting TFH and TFR cell differentiation. In addition, we find that PD-1 suppresses TFH cell differentiation and help for Ig class switching, even in the presence of wild-type TFR cells. Our work points to critical roles for PD-L1 expressed on DCs in mediating PD-1 functions.
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