Glucocorticoid prevents CD138 expression in T cells of autoimmune MRL/lpr mice

CD138(+) T cells, the majority of which are CD4 and CD8 double-negative (DN) T cells, contribute to the production of anti-dsDNA antibodies in a CD4 receptor-dependent way to promote the development of systemic lupus erythematosus (SLE). Accumulation of CD138(+) T cells in the spleen of MRL/lpr mice was significantly reduced by prednisone. Reduced expression of CD138 in DN T cells induced by prednisone treatment alleviated the accumulation of DN T cells in MRL/lpr mice. The frequency of CD138(+) cells in CD4(+) T cells of prednisone-treated MRL/lpr mice was also significantly reduced, which subsequently contributed to reduced production of anti-dsDNA antibody in the prednisone-treated MRL/lpr mice. Additionally, prednisone significantly reduced serum IgG and IgG subsets and simultaneously increased IgM secretion in serum. This suggested that glucocorticoids played a protective role during SLE treatment in MRL/lpr mice by promoting the production of IgM. The present study provides new insights into the mechanism of glucocorticoid for the treatment of SLE.