期刊
NATURE MEDICINE
卷 16, 期 4, 页码 452-U136出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.2106
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资金
- Canadian Institutes of Health Research (CIHR)
- Canadian Foundation for Infectious Diseases
- Fonds de la recherche en sante du Quebec
- US National Institutes of Health
- Canadian Foundation for AIDS Research
- Canadian Network for Vaccines and Immunotherapeutics
Viral replication and microbial translocation from the gut to the blood during HIV infection lead to hyperimmune activation, which contributes to the decline in CD4(+) T cell numbers during HIV infection. Programmed death-1 (PD-1) and interleukin-10 (IL-10) are both upregulated during HIV infection. Blocking interactions between PD-1 and programmed death ligand-1 (PD-L1) and between IL-10 and IL-10 receptor (IL-10R) results in viral clearance and improves T cell function in animal models of chronic viral infections. Here we show that high amounts of microbial products and inflammatory cytokines in the plasma of HIV-infected subjects lead to upregulation of PD-1 expression on monocytes that correlates with high plasma concentrations of IL-10. Triggering of PD-1 expressed on monocytes by PD-L1 expressed on various cell types induced IL-10 production and led to reversible CD4(+) T cell dysfunction. We describe a new function for PD-1 whereby microbial products inhibit T cell expansion and function by upregulating PD-1 levels and IL-10 production by monocytes after binding of PD-1 by PD-L1.
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