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CD103hi lung-resident regulatory T cells constrain the fibrotic responses induced by CD103low tissue-resident pathogenic CD4 T cells

ABSTRACT: CD103hi lung-resident regulatory T cells constrain the fibrotic responses induced by CD103low tissue-resident pathogenic CD4 T cells

PROVIDER: PRJNA551397 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9606480.fastq.gz	Fastqsanger.gz
	SRR9606490.fastq.gz	Fastqsanger.gz
	SRR9606500.fastq.gz	Fastqsanger.gz
	SRR9606481.fastq.gz	Fastqsanger.gz
	SRR9606491.fastq.gz	Fastqsanger.gz

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CD103hi lung-resident regulatory T cells constrain the fibrotic responses induced by CD103low tissue-resident pathogenic CD4 T cells

Project description:Tissue-resident memory T (TRM) cells are crucial mediators of adaptive immunity in non-lymphoid tissues. However, the functional heterogeneity and pathogenic roles of CD4+ TRM cells that reside within chronic inflammatory lesions remain unknown. We found that CD69hiCD103low CD4+ TRM cells produced effector cytokines and promoted the inflammation and fibrotic responses induced by chronic exposure to Aspergillus fumigatus. Simultaneously, immunosuppressive CD69hiCD103hiFoxp3+ CD4+ regulatory T (Treg) cells were induced and constrained the ability of pathogenic CD103low TRM cells to cause fibrosis. Thus, lung tissue-resident CD4+ T cells play crucial roles in the pathology of chronic lung inflammation, and CD103 expression defines pathogenic effector and immunosuppressive tissue-resident cell subpopulations in the inflamed lung.

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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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Project description:We isolated non-hematopoietic cells from fibrotic and non-fibrotic mouse bone marrow and perfomed scRNAseq on them. We identified 8 different stromal populations. Our analysis revealed two distinct mesenchymal stromal cells (MSC) subsets as pro-fibrotic cells. MSCs were functionally reprogrammed in a stagedependent manner with loss of their progenitor status and initiation of differentiation in the prefibrotic stage and acquisition of a pro-fibrotic and inflammatory phenotype in the fibrotic stage. In parallel, IL-33-expressing myelinating Schwann cell progenitors expanded, likely as a repair mechanism for the previously described neuropathy in MPN.

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2020-11-03 | GSE156640 | GEO

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