CD11c,FcRL5或T-bet通常在炎症过程中由B细胞扩增表达,它们可以构成>30%的成熟B细胞。然而,蛋白质与宿主反应中的分化和功能之间的关联仍不清楚。我们已经评估了CD11c的共表达,T-bet,和FcRL5在体外B细胞培养系统中确定如何通过BCR进行刺激,toll样受体9(TLR9),不同的细胞因子影响CD11c,T-bet,和FcRL5表达。我们观察到所有标志物的不同表达动态,但是在响应BCR和TLR9激活时,CD11c和FcRL5的调节大部分重叠,而T-bet强烈依赖于IFN-γ信号传导。研究浆细胞分化和APC功能,标记物表达与抗体分泌或T细胞帮助之间无关联.相反,这些功能与TLR9信号传导和B细胞衍生的IL-6产生有关,分别。这些结果表明,CD11c的表达,FcRL5和T-bet和浆细胞分化和改善的APC功能平行发生,并受相似的激活信号调节,但它们不是相互依存的。
CD11c,
FcRL5, or T-bet are commonly expressed by B cells expanding during inflammation, where they can make up >30% of mature B cells. However, the association between the proteins and differentiation and function in the host response remains largely unclear. We have assessed the co-expression of CD11c, T-bet, and
FcRL5 in an in vitro B-cell culture system to determine how stimulation via the BCR, toll-like receptor 9 (TLR9), and different cytokines influence CD11c, T-bet, and
FcRL5 expression. We observed different expression dynamics for all markers, but a largely overlapping regulation of CD11c and
FcRL5 in response to BCR and TLR9 activation, while T-bet was strongly dependent on IFN-γ signaling. Investigating plasma cell differentiation and APC functions, there was no association between marker expression and antibody secretion or T-cell help. Rather the functions were associated with TLR9-signalling and B-cell-derived IL-6 production, respectively. These results suggest that the expression of CD11c,
FcRL5, and T-bet and plasma cell differentiation and improved APC functions occur in parallel and are regulated by similar activation signals, but they are not interdependent.