To date, the mechanism of systemic lupus erythematosus (SLE) has not been thoroughly deciphered. Recent research demonstrated that CD138+ T cells accumulate in an SLE murine model, indicating that they are autoreactive T cells that significantly promote autoantibody production. Double negative (DN) T cells have been demonstrated to participate in the progression of SLE, but their detailed mechanism and the role in SLE remain unclear. Importantly, the expression of CD138 in CD3+ T cells plays a key role in the progression of lupus; it causes the accumulation of autoreactive T cells, including DN T cells, by significantly preventing their apoptosis. T helper 1 cells and interferon gamma both prevail in SLE; they may play essential roles in building the inflammatory condition of SLE. Defects occur in regulatory B (Breg) cells during their expansion in SLE, resulting in more differentiation of activated B cells into plasma cells; this subsequently increases antibody production. Myeloid-derived suppressor cells (MDSCs) enhance the expansion of Breg cells. However, the sustained increase of cytokine levels in SLE promotes the differentiation of more MDSCs into macrophage and dendritic cells, resulting in the defective expansion of MDSCs. The defective expansion of Breg cells and MDSCs breaks the immune-tolerance milieu in SLE, resulting in increased autoantibody secretion from those abnormal plasma cells. This review discusses recent advances regarding the detailed roles and mechanisms of these immunocytes in SLE.