Autoinflammatory & rare systemic diseases
Single‐Cell Profiling of Lymphoid and Myeloid Compartments Reveals Coordinated Immune Dysregulation and Enhanced Monocyte‐Centric Intercellular Communication in Relapsing Polychondritis
Authors' conclusion
This study delineates a comprehensive, cell type-revolved atlas of peripheral immune dysregulation in RP, revealing coordinated alterations in T cell activation and redistribution, B cell differentiation, myeloid-driven inflammation, and prominent alarmin-related signatures.
Study context
- Population
- Peripheral blood mononuclear cells from patients with relapsing polychondritis (RP) and matched healthy controls
- Participants
- 6 vs 5
- Comparison
- RP vs matched healthy controls
- RPn = 6
- Healthy controlsn = 5reference
- Outcome
- Peripheral immune landscape (scRNA-seq of PBMCs)
Methodological detailssingle-cell RNA sequencing, matched healthy controls
- Single-cell RNA sequencing
- Matched healthy controls
Main finding
As reported in the abstract
- Significant reduction in circulating T cells in RP
- Trend toward increased CD14+ monocytes, neutrophils and plasma cells
- Within T cells: expansion of CD8+ subsets; depletion of FCER1G+ T, γδT and mucosal-associated invariant T cells
- T-cell transcriptional programs indicating enhanced chemotaxis, activation, differentiation and interferon responses, with cytolytic ability in cytotoxic T subsets
- B cells: activated phenotype, increased plasma cell differentiation potential and metabolic reprogramming
- Myeloid cells: robust up-regulation of alarmins (S100A8/9/12) and proinflammatory pathways
- CD14+ monocytes as dominant signalling hubs (annexin, MHC, resistin, chemokine ligand-receptor pairs), with enrichment of the ANXA1-FPR1 axis
Original publication
Single‐Cell Profiling of Lymphoid and Myeloid Compartments Reveals Coordinated Immune Dysregulation and Enhanced Monocyte‐Centric Intercellular Communication in Relapsing Polychondritis. Arthritis Rheumatol. Published 11 August 2026. doi:10. 1002/ art. 70294
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