Effect of abnormal activated B cells in patients with ankylosing spondylitis and its molecular mechanism.

Abstract

Ankylosing spondylitis (AS) is a common clinical autoimmune disease, the pathogenesis of which, however, is not yet elucidated. In this study, we aim to explore the effect of B cells in the development and progression of AS and its underlying mechanism. B cells were isolated from peripheral blood of AS patients and normal controls. Surface expression of CD40 in B cells was detected by flow cytometry. Expressions of downstream genes in MAPK pathway were detected by Western blot. Moreover, IL-10 expressions in peripheral blood of AS patients and normal controls were detected by ELISA. No difference was found in the surface expression of CD40 in B cells between AS patients and normal controls. However, CD40 expression was inhibited after B cells in peripheral blood were specifically stimulated by lipopolysaccharide (LPS) in vitro. Abnormal activated B cells, dysregulated p38 expressions and decreased serum expressions of IL-10 were also observed in AS patients. Abnormal surface expression of CD40 inn B cells of AS patients may lead to abnormal activation of B cells, thereby interfering the p38 MAPK pathway and reducing the IL-10 secretion.