Abstract
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.