Background/Purpose: Abatacept, an efficacious therapy for rheumatoid arthritis (RA), inhibits the interaction between CD28 on T cells and CD80/CD86 on antigen-presenting cells (APCs). The aim of our study was to examine the effect of abatacept on B cell subtypes in patients with RA.

Methods: Twenty-five patients with RA, not responding to conventional DMARDs, received Abatacept and included in the study. DAS28 (ESR), DAS28(CRP) and SDAI were measured at baseline and at 6 months post-treatment. Serum sample and peripheral blood mononuclear cells were collected at baseline and at 6 months post-treatment. ACPA were tested using commercial ELISA and LINEBLOT (for CCP3, citrullinated vimentin, citrullinated a-enolase peptide). Five subsets of B cells including regulatory B cells (Bregs) were analyzed at baseline and 6-months post-Abatacept treatment by flow cytometry using a FACS Calibur cytometer (Becton Dickinson): B cells, naive B cells, PDL-1+B cells, PDL-1+CD27+B cells, PDL-1+CD27-B cells, PDL-1hiBregs (CD19+ PD-L1++).

Results: At baseline ACPA positivity was found in 52% of patients. All patients who were positive for ACPA at baseline remained positive at 6 months post-treatment without significant changes of their titers. In addition, none of ACPA-negative patients become positive at 6-months post-treatment. Response to therapy was found in 84.6% ACPA(+) patients and in 58.3% of ACPA(-) (p=0.0034). DAS28(ESR), DAS28(CRP) and SDAI scores at baseline were (mean±SD, 5.64±1.36, 5.19±1.40, and 34.13±18.23, respectively and significantly decreased at 6-months post-treatment (3.03±1.14, 2.9±1.02 and 9.06±7.82, respectively). At baseline, levels of B cell subtypes were higher in ACPA(+) compared to ACPA(-) patients (naïve Bregs, 44.89±11.48 vs 35.66±14.6, p=0.095; PDL1+B cells, 24.19±9.13 vs 17.7±5.73, p=0.044; PDL-1+ of CD27+B cells, 29.37±8.41 vs 18.45±7.13, p=0.002; PDL-1hiBregs, 7.64±2.29 vs 5.84±2.00, p=0.048). At 6 months post-treatment, ACPA(+) patients compared to ACPA(-) patients exhibited higher percentage increase in PDL-1+ of CD27-B cells (39.3±28.04 vs 14.45±18.87, p=0.016) and in PDL-1hiBregs cells (38.02±23.2 vs 12.9±15.38, p=0.004).High levels of B cell subtypes at baseline were associated with SDAI remission at 6 months post-Abatacept treatment. At baseline, responders compared to non-responders had higher levels of naïve B cells (45.01±10.37 vs 28.64±14.56, p=0.025), PDL-1+B cells (24.07±7.61 vs 13.4±3.3, p < 0.001), PDL-1+ of CD27+ B cells (27.51±8.51 vs 15.44±5.58, p=0.001), and PDL-1hiBregs (7.69±1.94 vs 4.40±1.25, p < 0.001). At 6-months post-treatment PDL-1+ of CD27-Bcells increased in responders vs non-responders (36.26±26.13% vs 4.52±9.39, p < 0.001). Finally, DAS28(ESR) score during treatment was negatively correlated with change of levels of PDL-1+CD27-B cells (p=0.029, r=-0.437).

Conclusion: In patients with RA treated with Abatacept, remission was higher in ACPA(+) than ACPA(-) patients. High levels of B cell subtypes at baseline were associated with SDAI remission at 6 months. DAS28(ESR) score during treatment was negatively correlated with PDL-1+CD27-B cells.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/changes-of-b-cell-subsets-during-treatment-with-abatacept-in-patients-with-rheumatoid-arthritis/