Lupus & antiphospholipid syndrome
Type I Interferon Drives Dysfunction of a Distinct CD8 + HLA ‐ DRB1 + T Cell Subset in Systemic Lupus Erythematosus
Authors' conclusion
CD8+ HLA-DRB1+ T cells represent a dysfunctional effector memory and proliferative population expanded in SLE. Type I IFN drives this paradoxical state by promoting exhaustion and impairing degranulation.
Study context
- Population
- Peripheral blood CD8+ T cells from patients with systemic lupus erythematosus (SLE) and healthy controlsscRNA-seq: 6 SLE, 6 matched controls
- Participants
- 11 vs 12
- Comparison
- SLE vs healthy controls
- SLEn = 11
- Healthy controlsn = 12reference
- Outcome
- CD8+ HLA-DRB1+ T cells
Methodological detailsflow cytometry, single-cell RNA sequencing, T cell receptor sequencing, IFNα stimulation
- Flow cytometry
- Single-cell RNA sequencing
- T cell receptor sequencing
- IFNα stimulation
Main finding
As reported in the abstract
- Enriched within effector memory, CD45RA+ effector memory and proliferative CD8+ T cells; significantly expanded within effector memory and proliferative compartment in SLE vs healthy controls
- Paradoxical features of cytotoxicity, proliferation, exhaustion and senescence
- Lupus cells vs healthy controls: increased exhaustion, reduced cytotoxicity, impaired antiviral pathways
- IFNα enhanced IFNγ responses and exacerbated exhaustion and senescence in lupus CD8+ HLA-DRB1+ T cells
- IFNα reduced CD107a surface mobilization (impaired degranulation) despite up-regulated cytotoxic gene expression
- Most kidney-infiltrating CD8+ T cells in LN data sets are HLA-DRB1+
- HLA-DRB1 expression on peripheral CD8+ T cells in SLE positively correlated with SLEDAI scores
Original publication
Type I Interferon Drives Dysfunction of a Distinct CD8 + HLA ‐ DRB1 + T Cell Subset in Systemic Lupus Erythematosus. Arthritis Rheumatol. Published 10 August 2026. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →