期刊
CELL
卷 171, 期 4, 页码 795-+出版社
CELL PRESS
DOI: 10.1016/j.cell.2017.09.052
关键词
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资金
- American Cancer Society
- NIH Medical Scientist Training Program grant [T32GM07739]
- NHMRC Fellowship [1119298]
- NHMRC [1125357, 1071822]
- Ludwig Center for Cancer Immunotherapy
- Burroughs Wellcome Fund
- NIH [AI100874, AI130043, P30CA008748]
- National Health and Medical Research Council of Australia [1125357, 1119298, 1071822] Funding Source: NHMRC
Infection is restrained by the concerted activation of tissue-resident and circulating immune cells. Whether tissue-resident lymphocytes confer early antiviral immunity at local sites of primary infection prior to the initiation of circulating responses is not well understood. Furthermore, the kinetics of initial antiviral responses at sites of infection remain unclear. Here, we show that tissue-resident type 1 innate lymphoid cells (ILC1) serve an essential early role in host immunity through rapid production of interferon (IFN)-gamma following viral infection. Ablation of Zfp683-dependent liver ILC1 lead to increased viral load in the presence of intact adaptive and innate immune cells critical for mouse cytomegalovirus (MCMV) clearance. Swift production of interleukin (IL)-12 by tissue-resident XCR1(+) conventional dendritic cells (cDC1) promoted ILC1 production of IFN-gamma in a STAT4-dependent manner to limit early viral burden. Thus, ILC1 contribute an essential role in viral immunosurveillance at sites of initial infection in response to local cDC1-derived proinflammatory cytokines.
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