期刊
NATURE IMMUNOLOGY
卷 20, 期 8, 页码 1004-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41590-019-0430-1
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资金
- National Institutes of Health (NIH) Medical Scientist Training Program training grant [T32GM007205]
- Medical Scientist Training Program grant from the National Institute of General Medical Sciences of the NIH [T32GM007739]
- National Institute of Allergy and Infectious Diseases of the NIH [F30 AI136239]
- Ludwig Center for Cancer Immunotherapy
- Burroughs Wellcome Fund
- American Cancer Society
- NIH [P30DK063491, AI145997, AI100874, AI130043, P30CA008748]
Innate lymphoid cells (ILCs) are tissue-resident sentinels that are essential for early host protection from pathogens at initial sites of infection. However, whether pathogen-derived antigens directly modulate the responses of tissue-resident ILCs has remained unclear. In the present study, it was found that liver-resident type 1 ILCs (ILC1s) expanded locally and persisted after the resolution of infection with mouse cytomegalovirus (MCMV). ILC1s acquired stable transcriptional, epigenetic and phenotypic changes a month after the resolution of MCMV infection, and showed an enhanced protective effector response to secondary challenge with MCMV consistent with a memory lymphocyte response. Memory ILC1 responses were dependent on the MCMV-encoded glycoprotein m12, and were independent of bystander activation by proinflammatory cytokines after heterologous infection. Thus, liver ILC1s acquire adaptive features in an MCMV-specific manner.
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