Exhausted-like CD8 resident memory T cells balance immunity and fibrotic sequelae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA476002 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7310672_1.fastq.gz | Fastqsanger.gz | |||
| SRR7310672_2.fastq.gz | Fastqsanger.gz | |||
| SRR7310673_1.fastq.gz | Fastqsanger.gz | |||
| SRR7310673_2.fastq.gz | Fastqsanger.gz |
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Project description:CD8 tissue-resident memory T cells (TRM) provide frontline immunity in mucosal tissues. The mechanisms regulating CD8 TRM maintenance, heterogeneity, protective and pathological functions are largely elusive. Here we identify an epitope-specific CD8 TRM population that is maintained by in situ MHC-I and B7 signaling following acute influenza infection. These TRM cells co-exhibit exhausted-like phenotypes and memory features, and provide heterologous immunity against secondary infection. PD-L1 blockade at the memory stage promotes exhausted-like TRM rejuvenation and secondary immunity at the cost of developing post-infection fibrotic sequelae. Increased numbers of CD8 TRM cells are observed in the lungs of pulmonary fibrosis patients compared to control patients. Thus, TRM exhaustion results from a tissue-specific cellular adaptation to balance fibrotic sequelae and secondary immunity.
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