The progressive damage in rheumatoid arthritis (RA) has been linked to an increase in inflammatory Th1/Th17 cells and a decrease in number or function of immunomodulatory regulatory T cells (Tregs). Many therapies that are effective in RA are shown to affect Th1/Th17 cells and/or Tregs. One such therapy, abatacept, utilizes a physiologic immunomodulatory molecule called cytotoxic lymphocyte antigen-4 (CTLA-4) which causes contact-dependent inhibition of inflammatory T-cell activation. Recent advances in CTLA-4 research has uncovered the method by which this occurs physiologically but the actions of the CTLA-4Ig fusion protein are still not fully understood. The reported effects of the drug on Treg population number and suppressor function have been very mixed. In this review, we will discuss the current literature surrounding the effects of abatacept in rheumatoid arthritis and explore potential explanations for the differences in results. Future opportunities in this area include contributions to a unified definition for different immune cell populations, LAG3⁺ Tregs which may pose an avenue for further study or the stratification of patients with regards to their specific disease characteristics, resulting in optimized treatment for disease remission.

类风湿性关节炎（RA）的进行性损害与炎症性Th1 / Th17细胞的增加以及免疫调节性T细胞（Tregs）数量或功能的降低有关。在RA中有效的许多疗法均显示会影响Th1 / Th17细胞和/或Treg。一种这样的疗法，即abatacept，利用一种称为细胞毒性淋巴细胞抗原4（CTLA-4）的生理免疫调节分子，该分子可引起炎症性T细胞活化的接触依赖性抑制。CTLA-4研究的最新进展揭示了在生理上发生这种现象的方法，但仍未完全了解CTLA-4Ig融合蛋白的作用。药物对Treg数量和抑制功能的报道影响很大。在这篇评论中 我们将讨论有关阿巴西普在类风湿关节炎中作用的最新文献，并探讨结果差异的潜在解释。该领域的未来机会包括为不同免疫细胞群LAG3的统一定义做出贡献⁺ Treg可能会为进一步研究或根据患者的特定疾病特征对患者进行分层，从而为疾病缓解提供优化的治疗方法。