Background B-cells are thought to have an important role in rheumatoid arthritis (RA). This is demonstrated by the success of B-cell depleting therapy as well as the negative prognostic value of anti-citrullinated protein antibodies (ACPA)¹. However, the pathogenesis of the disease is unclear. Studies have suggested that there are differences in disease characteristics between elderly-onset RA patients (EORA, defined by disease onset at ≥60 years of age) and younger-onset RA patients (YORA, with disease onset <60 years of age).²

Objectives Our aim was to study the B-cell subpopulations in newly diagnosed EORA and YORA patients. We investigated whether there were differences in B-cell subpopulations between the groups and whether there was a correlation between B-cell subpopulations and disease activity, autoantibody profile and inflammatory parameters in these two RA patient groups.

Methods Treatment-naive EORA (n=29) and Yora (n=31) patients with newly diagnosed RA were included at their first visit to the Rheumatology clinic. The patients’ clinical response (DAS28), autoantibodies and B-cells were assessed. Flow cytometry was used for the analysis of cellular surface markers on leukocytes in peripheral blood: CD19, CD27, CD24, CD27, CD38, PD-1, PD-L1, IgG, IgD and IgM. Non-parametric tests were used for comparing groups and Spearman’s test was used for correlation.

Results We found a correlation between the ACPA titers and the frequency of the CD27⁺ and CD27^- memory B cell populations in EORA patients but not in YORA patients. This was further supported by a correlation of the ACPA titer and IgG⁺ B cells in the EORA patients (r=0.7, p=0.003) and not in the YORA patients. There was neither a correlation between age and ACPA titer nor between age and memory B cell populations. We did not find any significant difference between the B cell subpopulations in the two patient groups.

Conclusions Our results suggest that the memory B cell compartment in peripheral blood in EORA patients reflects the ACPA titer. This was not seen in the YORA patients. The mechanisms behind these findings need to be further elucidated.

References [1] Bugatti S, Vitolo B, Caporali R, Montecucco C, Manzo A. B cells in rheumatoid arthritis: from pathogenic players to disease biomarkers. Biomed Res Int2014;2014:681678.

[2] Kobak S, Bes C. An autumn tale: geriatric rheumatoid arthritis. Ther Adv Musculoskelet Dis2018;10:3–11.

Disclosure of Interest None declared