期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 120, 期 7, 页码 2508-2515出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI40040
关键词
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资金
- NIH [AI56299, AI30048, AI04464409, T32 HL007627]
- Gates Foundation Grand Challenges in Global Health
- Ministry for Health, Welfare & Family Affairs, Republic of Korea [A091204]
- Korea Health Promotion Institute [A091204] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
The inhibitory receptor programmed death 1 (PD-1) is upregulated on antigen-specific CD8(+) T cells during persistent viral infections. Interaction with PD-1 ligand 1 (PD-L1) contributes to functional exhaustion of responding T cells and may limit immunopathology during infection. PD-L1 is expressed on both hematopoietic and nonhematopoietic cells in tissues. However, the exact roles of PD-L1 on hematopoietic versus nonhematopoietic cells in modulating immune responses are unclear. Here we used bone marrow chimeric mice to examine the effects of PD-L1 deficiency in hematopoietic or nonhematopoietic cells during lymphocytic choriomeningitis virus clone 13 (LCMV CL-13) infection. We found that PD-L1 expression on hematopoietic cells inhibited CD8(+) T cell numbers and function after LCMV CL-13 infection. In contrast, PD-L1 expression on nonhematopoietic cells limited viral clearance and immunopathology in infected tissues. Together, these data demonstrate that there are distinct roles for PD-L1 on hematopoietic and nonhematopoietic cells in regulating CD8(+) T cell responses and viral clearance during chronic viral infection.
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