期刊
SCIENCE IMMUNOLOGY
卷 5, 期 53, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciimmunol.abc4557
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资金
- U.S. National Institutes of Health [AI112844, AI147394, AG069264, AG047156, NS103212, AI125701, AI139721, HL52160, T32AG04967]
- Mayo Clinic CBD Research Fund
- Cancer Research Institute CLIP program [RSG-18-222-01-LIB]
- American Cancer Society [RSG-18-222-01-LIB]
- Three Lakes Partners Foundation
Lower respiratory viral infections, such as influenza virus and severe acute respiratory syndrome coronavirus 2 infections, often cause severe viral pneumonia in aged individuals. Here, we report that influenza viral pneumonia leads to chronic nonresolving lung pathology and exacerbated accumulation of CD8(+) tissue-resident memory T cells (T-RM) in the respiratory tract of aged hosts. T-RM cell accumulation relies on elevated TGF-beta present in aged tissues. Further, we show that T-RM cells isolated from aged lungs lack a subpopulation characterized by expression of molecules involved in TCR signaling and effector function. Consequently, T-RM cells from aged lungs were insufficient to provide heterologous protective immunity. The depletion of CD8(+) T-RM cells dampens persistent chronic lung inflammation and ameliorates tissue fibrosis in aged, but not young, animals. Collectively, our data demonstrate that age-associated T-RM cell malfunction supports chronic lung inflammatory and fibrotic sequelae after viral pneumonia.
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