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

Publication date: Available online 19 December 2018

Source: Clinical Immunology

Author(s): Maiko Yoshikawa, Shingo Nakayamada, Satoshi Kubo, Aya Nawata, Yukihiro Kitanaga, Shigeru Iwata, Kei Sakata, Ma Xiaoxue, Sheau Pey Wang, Kazuhisa Nakano, Kazuyoshi Saito, Yoshiya Tanaka

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.

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