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Single cell analysis reveals multiple subsets of CD8+ TRM and non-TRM cells with a type 17 signature in the inflamed psoriatic arthritis joint

ABSTRACT: Single cell analysis reveals multiple subsets of CD8+ TRM and non-TRM cells with a type 17 signature in the inflamed psoriatic arthritis joint

PROVIDER: PRJNA896174 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22107931.fastq.gz	Fastqsanger.gz
	SRR22107932.fastq.gz	Fastqsanger.gz
	SRR22107933.fastq.gz	Fastqsanger.gz
	SRR22107934.fastq.gz	Fastqsanger.gz
	SRR22107935.fastq.gz	Fastqsanger.gz

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Single cell analysis reveals multiple subsets of CD8+ TRM and non-TRM cells with a type 17 signature in the inflamed psoriatic arthritis joint

Project description:CD69+CD103+ tissue-resident memory T-cells (TRM) are increasingly recognised as important drivers of inflammation. To decipher their potential role in inflammatory arthritis, we applied single cell, high-dimensional profiling (CyTOF and scRNAseq) to T-cells isolated from the joint of patients with psoriatic arthritis (PsA) or rheumatoid arthritis (RA). We identified three broad groups of synovial CD8+ TRM cells: cytotoxic and Treg-like TRM cells were present in the inflamed joints of patients with both PsA and RA, while CD161+CXCR6+ type 17-like TRM cells with a pro-inflammatory cytokine profile (IL-17A+TNFa+IFNg+) and a distinct transcriptomic signature and a polyclonal, but distinct TCR repertoire, were specifically enriched in the inflamed joints of patients with PsA. Type 17-like cells were also enriched in non-TRM CD8+ T-cells in PsA compared to RA. These findings add substantively to the accumulating evidence that the immunopathology of PsA and RA is different, with a particular role for type 17 cells in PsA.

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Clonal sharing of CD8+ T-cells links skin and joint inflammation in psoriatic arthritis

Project description:We hypothesised that skin and joint inflammation in psoriatic arthritis is linked in terms of CD8+ T-cell phenotype and clonality. We employed scRNAseq to directly compare the transcriptional signature and T-cell receptor repertoire of memory T-cells from paired skin and synovial tissue+/-fluid from patients with psoriatic arthritis. We identified an enrichment of type-17 CD8+ tissue-resident memory (TRM) cells in both skin and joint, with a stronger IL-17 signature in the skin than the joint. Importantly, we identified several T-cell clones that are shared between the skin and the joint. Shared clones tended to have the same phenotype at both sites, characterised by increased expression of genes associated with a cytotoxic, tissue-resident phenotype. This supports the hypothesis that skin and joint inflammation is linked in terms of T-cell clonality and raises the possibility that specific T-cells migrate between these compartments to propagate inflammation across both sites.

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Arthritis Flares Mediated by Tissue Resident Memory T Cells in the Joint

Project description:Rheumatoid arthritis is a systemic autoimmune disease, but disease flares typically affect only a subset of joints, distributed in a pattern that is distinctive for each patient. Pursuing this intriguing pattern, we show that arthritis recurrence is mediated by long-lived synovial resident memory T cells (TRM). In three murine models, CD8+ cells bearing TRM markers remain in previously inflamed joints during remission. These cells are bona fide TRM, exhibiting failure to migrate from joint to joint, preferential uptake of fatty acids, and long-term residency. Disease flares result from TRM activation by antigen, leading to CCL5-mediated recruitment of circulating effector cells. Correspondingly, TRM depletion ameliorates recurrence in a site-specific manner. Human rheumatoid arthritis joint tissues contain a comparable CD8+-predominant TRM population, most evident in late-stage leukocyte-poor synovium, exhibiting limited T cell receptor diversity and a pro-inflammatory transcriptomic signature. Together, these findings establish synovial TRM cells as a targetable mediator of disease chronicity in autoimmune arthritis.

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