Type I and II interferons commit to abnormal expression of chemokine receptor on B cells in patients with systemic lupus erythematosus

Abstract Memory B cells are increased in systemic lupus erythematosus (SLE) cases, but the qualitative abnormalities and induction mechanism of these cells are unclear. Here, we subclassified B cells by their chemokine receptor expression and investigated their induction mechanism. The peripheral blood of patients with SLE showed higher levels of CXCR5 − and CXCR3 + B cells. CXCR5 − CXCR3 + B cell levels were elevated in patients with active SLE, which decreased with improving disease conditions. Interferon (IFN)-γ stimulation increased CXCR3 expression, whereas IFN-β stimulation reduced CXCR5 expression in B cells. Furthermore, CXCR5 − CXCR3 + B cells were induced by a combination of IFN-β and IFN-γ stimulation. Renal tissue examination of patients with active lupus nephritis confirmed the presence of CD19 + CXCR3 + B cells. Collectively, the results revealed qualitative abnormalities accompanying reduced CXCR5 expression via type I IFN and enhanced CXCR3 expression via type II IFN in SLE, suggesting their involvement in B cell infiltration into tissues and inflammatory pathogenesis.