期刊
CELL HOST & MICROBE
卷 11, 期 6, 页码 631-642出版社
CELL PRESS
DOI: 10.1016/j.chom.2012.05.003
关键词
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资金
- National Heart, Lung, and Blood Institute [2T32HL007317-31]
- NRSA from the National Institute of Diabetes and Digestive and Kidney Diseases [5T32DK007296]
- NIAID Center for HIV/AIDS Vaccine Immunology [A1067854]
Type I interferon (IFN-I) promotes antiviral CD8(+)T cell responses, but the contribution of different IFN-I sources and signaling pathways are ill defined. While plasmacytoid dendritic cells (pDCs) produce IFN-I upon TLR stimulation, IFN-I is induced in most cells by helicases like MDA5. Using acute and chronic lymphocytic choriomeningitis virus (LCMV) infection models, we determined that pDCs transiently produce IFN-I that minimally impacts CD8(+)T cell responses and viral persistence. Rather, MDA5 is the key sensor that induces IFN-I required for CD8(+)T cell responses. In the absence of MDA5, CD8(+)T cell responses to acute infection rely on CD4(+)T cell help, and loss of both CD4(+)T cells and MDA5 results in CD8(+)T cell exhaustion and persistent infection. Chronic LCMV infection rapidly attenuates IFN-I responses, but early administration of exogenous IFN-I rescues CD8(+)T cells, promoting viral clearance. Thus, effective antiviral CD8(+)T cell responses depend on the timing and magnitude of IFN-I production.
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