Systemic sclerosis & Raynaud's
Dysfunctional KLRB1+CD8+ T-cell responses are generated in chronically inflamed systemic sclerosis skin
Authors' conclusion
This study provides new insight into core regulatory programmes modulating skin-resident CD8+ T-cell plasticity and identifies distinct CD8+ T-cell subpopulations that contribute to initiation and chronicity of inflammatory responses in systemic sclerosis skin lesions.
Study context
- Population
- Patients with diffuse cutaneous systemic sclerosis (dcSSc); well-characterised patient skin samples
- Comparison
- SSc skin lesions vs healthy control skin
- Outcome
- Skin-resident CD8+ T-cell subsets
Methodological detailssingle-cell transcriptomics and epigenomics, multicolor immunofluorescence microscopy, ex vivo skin explant assays
- Single-cell transcriptomics and epigenomics
- Multicolor immunofluorescence microscopy
- Ex vivo skin explant assays
Main finding
As reported in the abstract
- 2 major developmentally connected CD8+ T-cell subpopulations expanded in SSc skin lesions vs healthy control skin
- Effector-memory CD8+KLRB1+IL7R+ subset with increased cytolytic and Tc2/Tc17 effector functions, appearing to induce tissue damage and fibrosis in early-stage dcSSc skin lesions
- Exhausted CD8+KLRG1+IL7R- subset, primarily in late-stage disease, with transcriptional features of long-lived effector cells, likely contributing to chronic inflammation
- Both subsets also expanded in other benign dermatoses
Original publication
Dysfunctional KLRB1+CD8+ T-cell responses are generated in chronically inflamed systemic sclerosis skin. Ann Rheum Dis. Published 1 February 2025. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →