Introduction
Systemic lupus erythematosus (SLE) is an autoimmune disease that is characterized by the production of multiple autoantibodies, including anti-nuclear antibody (ANA) and anti-double-stranded deoxyribonucleic acid (dsDNA) antibody 1, 2. The production of these autoantibodies detrimentally affects multiple tissues and organs3-5. It is believed that B cells play central roles in adaptive immune responses as they specialize in the production of antibodies. However, SLE has so much variability and complexity that both T and B cells participate in the progress of SLE6-8.
Despite the mechanism of SLE being so complex and unclear, recent research has achieved some advances. It has been demonstrated that double negative (DN) T cells accumulate significantly in both lupus mice and SLE patients 9-11, but the mechanism of this accumulation has not yet been thoroughly deciphered. Recent research reveals that the majority of accumulated DN T cells express CD138 in lupus mice, and that the expression of CD138 decrease the level of apoptosis in CD3+ T cells, compared with that in CD3+CD138- T cells12-14. In addition, other immunocytes, such as myeloid-derived suppressor cells (MDSCs), T helper 1 (Th1) cells, and regulatory B (Breg) cells have also been found to participate in SLE. Here, we discuss recent developments and research advances regarding the mechanisms underlying the immune system function in SLE.