Chisato Ono, Yuta Kochi, Yoshihiro Baba, Shinya Tanaka
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引用次数: 0
摘要
B细胞的初始活性是通过B细胞中表达的调控分子介导的激活和抑制的平衡来调节的;然而,这一过程的分子机制仍不完全清楚。在这项研究中,我们研究了 Fc 受体样(Fcrl)家族分子 Fcrl5 在体液免疫反应中的功能。我们的研究表明,B细胞特异性过表达Fcrl5能增强T细胞依赖型1(TI1)和T细胞依赖型(TD)反应中抗体(Ab)的产生。此外,在 TD 反应的竞争条件下,它还能促进效应 B 细胞的形成。从机理上讲,体外激动性 Abs 与 Fcrl5 连接可减少细胞死亡,并增强脂多糖(LPS)刺激下 B 细胞的增殖。在抗CD40 Abs和IL-5存在的情况下,Fcrl5结扎不仅能抑制细胞死亡,还能促进分化成浆细胞。这些发现揭示了 Fcrl5 在通过增强 B 细胞活力和浆细胞分化促进体液免疫反应中的新作用。
Humoral responses are enhanced by facilitating B cell viability by Fcrl5 overexpression in B cells.
B cell initial activity is regulated through a balance of activation and suppression mediated by regulatory molecules expressed in B cells; however, the molecular mechanisms underlying this process remain incompletely understood. In this study, we investigated the function of the Fc receptor-like (Fcrl) family molecule Fcrl5, which is constitutively expressed in naive B cells, in humoral immune responses. Our study demonstrated that B cell-specific overexpression of Fcrl5 enhanced antibody (Ab) production in both T cell-independent type 1 (TI1) and T cell-dependent (TD) responses. Additionally, it promoted effector B cell formation under competitive conditions in TD responses. Mechanistically, in vitro ligation of Fcrl5 by agonistic Abs reduced cell death and enhanced proliferation in lipopolysaccharide-stimulated B cells. In the presence of anti-CD40 Abs and IL-5, the Fcrl5 ligation not only suppressed cell death but also enhanced differentiation into plasma cells. These findings reveal a novel role of Fcrl5 in promoting humoral immune responses by enhancing B cell viability and plasma cell differentiation.
期刊介绍:
International Immunology is an online only (from Jan 2018) journal that publishes basic research and clinical studies from all areas of immunology and includes research conducted in laboratories throughout the world.