期刊
SCIENCE IMMUNOLOGY
卷 4, 期 36, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciimmunol.aaw1217
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资金
- NIH [RO1 AI112844, RO1 AG047156, RO1 HL126647, T32AG049672, R01 HL62150]
- NHLBI [268201600004I-0-26800001-1, R01 AI057459, R01 AI129241, R56 NS094150, R01 NS103212, RO1 AI125701, R21 AI139721, R01HL122559]
- Huvis Foundation
- Mayo Clinic Kogod Aging Center Pilot grant
- Mayo Clinic Center for Biomedical Discovery discretionary fund
- CRI (Cancer Research Institute) Clinic and Laboratory Integration Program
CD8(+) tissue-resident memory T (T-RM) cells provide frontline immunity in mucosal tissues. The mechanisms regulating CD8(+) T-RM maintenance, heterogeneity, and protective and pathological functions are largely elusive. Here, we identify a population of CD8(+) T-RM cells that is maintained by major histocompatibility complex class I (MHC-I) signaling, and CD80 and CD86 costimulation after acute influenza infection. These T-RM cells have both exhausted-like phenotypes and memory features and provide heterologous immunity against secondary infection. PD-L1 blockade after the resolution of primary infection promotes the rejuvenation of these exhausted-like T-RM cells, restoring protective immunity at the cost of promoting postinfection inflammatory and fibrotic sequelae. Thus, PD-1 serves to limit the pathogenic capacity of exhausted-like T-RM cells at the memory phase. Our data indicate that T-RM cell exhaustion is the result of a tissue-specific cellular adaptation that balances fibrotic sequelae with protective immunity.
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