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Systemically primed central memory T cells source intranasally boosted tissue-resident memory T cells against melanoma lung metastasis

ABSTRACT: Tissue resident memory T (TRM) cells mediate the frontline protection against melanoma lung metastasis. We utilized scRNA-seq to investigate the underlying molecular mechanism of central memory T (TCM) to lung TRM development in the prime-boost vaccinaiton regimen.

ORGANISM(S): Mus musculus

PROVIDER: GSE238223 | GEO | 2024/07/10

REPOSITORIES: GEO

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Single cell CITE-seq and VDJ sequencing of CD8+ central memory blood T cells (TCM) and their in-vivo matured tissue-resident memory-like T cells (TRM)

Project description:The aim of the experiment was to understand the clonal relationship between CD8+ central memory blood T cells (TCM) and the in-vivo matured TCM tissue-resident memory-like T cells (TRM) on day 14. TCM were FACS sorted from human PBMCs (n=5). Half of the cells were processed on day 1 and half of the cells of each donor were matured into TRM with anti-CD3, IL-15 and TGF beta for 14 days. Both day 1 TCM and matured day 14 TRM-like cells were further processed using the 5´10X genomics workflow.

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Systemically primed central memory T cells source intranasally boosted tissue-resident memory T cells against melanoma lung metastasis

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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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