Vasculitis & polymyalgia rheumatica
Age‐Associated B Cells Contribute to Inflammation Via Antibody‐Independent Mechanisms in Takayasu Arteritis
Authors' conclusion
ABCs promote inflammation through proinflammatory functions independent of ASC differentiation in TAK. JAK inhibition exerts distinct suppressive effects on ABCs compared with anti-TNF therapy.
Study context
- Population
- Patients with TAK, compared with systemic lupus erythematosus (SLE) (cross-data set)
Methodological detailshistologic analysis, bulk RNA-seq, single-cell RNA-seq, flow cytometry, in vitro experiments, exploratory clinical follow-up
- Histologic analysis
- Bulk RNA-seq
- Single-cell RNA-seq
- Flow cytometry
- In vitro experiments
- Exploratory clinical follow-up
Main finding
As reported in the abstract
- Extrafollicular response and up-regulated age-associated B cell (ABC) production in TAK (histologic n = 5, flow cytometric n = 125, bulk RNA-seq n = 12)
- Transcriptomic differences between B cells from TAK and SLE (cross-data set)
- ABC differentiation in TAK largely uncoupled from antibody-secreting cell (ASC) generation, unlike SLE (single-cell RNA-seq (scRNA-seq); in vitro n = 5)
- ABCs proinflammatory, incl. proinflammatory cytokine production; CD11c+ B cells promoted Th17 cell differentiation (n = 6)
- In vitro, tofacitinib more effective than adalimumab at reducing ABC proportions and attenuating their proinflammatory phenotype (n = 15), consistent with trends in exploratory clinical follow-up (n = 4)
Original publication
Age‐Associated B Cells Contribute to Inflammation Via Antibody‐Independent Mechanisms in Takayasu Arteritis. Arthritis Rheumatol. Published 4 August 2026. doi:10.
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