CD20⁺ T cells comprise a highly inflammatory subset implicated in autoimmunity, including rheumatoid arthritis (RA). We sought to characterize the CD20⁺ T cell subset in the murine collagen-induced arthritis (CIA) model of RA and investigate the phenotype and functional relevance of CD3⁺CD20⁺ T cells in the lymph nodes and arthritic joints using flow cytometry and immunohistochemistry. We demonstrate that CD3⁺CD4⁺CD20⁺ and CD3⁺CD8⁺CD20⁺ T cells are expanded in the draining lymph nodes of CIA mice, produce increased levels of pro-inflammatory cytokines and are less susceptible to regulation by regulatory T cells. Notably, CD3⁺CD4⁺CD20⁺ and CD3⁺CD8⁺CD20⁺ T cells are enriched with CXCR5⁺PD-1⁺ T follicular helper cells and CXCR5^-PD-1⁺ peripheral T helper cells, subsets of T cells implicated in promoting B-cell responses and antibody production within pathologically inflamed non-lymphoid tissues in RA. Our findings suggest CD20⁺ T cells are associated with inflammatory responses and may exacerbate pathology by promoting inflammatory B-cell responses.

CD20 ⁺ T 细胞包含与自身免疫相关的高度炎症亚群，包括类风湿性关节炎 (RA)。我们试图表征RA 鼠胶原诱导关节炎 (CIA) 模型中的CD20 ⁺ T 细胞亚群，并使用流式细胞术和免疫组织化学研究淋巴结和关节炎关节中CD3 ⁺ CD20 ^{+ T 细胞的表型和功能相关性。}我们证明 CD3 ⁺ CD4 ⁺ CD20 ⁺和 CD3 ⁺ CD8 ⁺ CD20 ⁺T 细胞在 CIA 小鼠的引流淋巴结中扩增，产生更高水平的促炎细胞因子，并且不易受到调节性 T 细胞的调节。值得注意的是，CD3 ⁺ CD4 ⁺ CD20 ⁺和 CD3 ⁺ CD8 ⁺ CD20 ⁺ T 细胞富含 CXCR5 ⁺ PD-1 ⁺ T 滤泡辅助细胞和 CXCR5 ^- PD-1 ⁺外周 T 辅助细胞，这些 T 细胞亚群涉及促进 B - RA 病理性发炎非淋巴组织内的细胞反应和抗体产生。我们的研究结果表明 CD20 ⁺T 细胞与炎症反应相关，并可能通过促进炎症 B 细胞反应而加剧病理学。