Aberrant pro-inflammatory responses of CD20+T cells in experimental arthritis

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.

Automated summary

CD20+ T cells are an inflammatory subset involved in autoimmune diseases, including rheumatoid arthritis (RA). In this study, we examined the characteristics of the CD20+ T cell subset in a murine model of RA and investigated the phenotype and function of CD3+CD20+ T cells in the lymph nodes and arthritic joints. We found that CD3+CD4+CD20+ and CD3+CD8+CD20+ T cells were expanded in the draining lymph nodes of the RA model, produced higher levels of pro-inflammatory cytokines, and were less regulated by regulatory T cells. These CD20+ T cells were also enriched with T follicular helper cells and peripheral T helper cells, which are involved in promoting B-cell responses and antibody production within inflamed non-lymphoid tissues in RA. Our findings suggest that CD20+ T cells contribute to inflammatory responses and may worsen pathology by promoting inflammatory B-cell responses.