期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 192, 期 7, 页码 1027-1034出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.192.7.1027
关键词
binding; proliferation inhibition; cytokine secretion inhibition; tissue expression; peripheral tolerance
资金
- NCI NIH HHS [CA84500, R01 CA084500] Funding Source: Medline
- NIAID NIH HHS [AI41584, P01 AI039671, AI39671] Funding Source: Medline
PD-1 is an immunoinhibitory receptor expressed by activated T cells, B cells, and myeloid cells. Mice deficient in PD-1 exhibit a breakdown of peripheral tolerance and demonstrate multiple autoimmune features. We report here that the ligand of PD-1 (PD-LI) is a member of the B7 gene family. Engagement of PD-1 by PD-L1 leads to the inhibition of T cell rcceptor-mediated lymphocyte proliferation and cytokine secretion. In addition, PD-1 signaling can inhibit at least suboptimal levels of CD28-mediated costimulation. PD-L1 is expressed by antigen-presenting cells, including human peripheral blood monocytes stimulated with interferon gamma, and activated human and murine dendritic cells. In addition, PD-L1 is expressed in nonlymphoid tissues such as heart and lung. The relative levels of inhibitory PD-L1 and costimulatory B7-1/B7-2 signals on antigen-presenting cells may determine the extent of T cell activation and consequently the threshold between tolerance and autoimmunity. PD-L1 expression on nonlymphoid tissues and its potential interaction with PD-1 may subsequently determine the extent of immune responses at sites of inflammation.
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