Dectin-1 Stimulation Selectively Reinforces LPS-driven IgG1 Production by Mouse B Cells.

Dectin-1 Stimulation Selectively Reinforces LPS-driven IgG1 Production by Mouse B Cells.
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DOI:
10.4110/in.2013.13.5.205
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发表时间:
2013-10
期刊:
影响因子:
6
通讯作者:
Park SR
Park SR
中科院分区:
医学3区
文献类型:
--
作者:
Seo BS;Lee SH;Lee JE;Yoo YC;Lee J;Park SR

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Dectin-1是一种非Toll样受体(non-Toll-like receptor,TLR)模式识别受体,是C型凝集素受体(C-type lectin receptor,CLR)的代表,特异性识别真菌细胞壁的β-葡聚糖。Dectin-1在先天性免疫细胞如树突状细胞和巨噬细胞中的重要性以前已经得到了很好的研究。然而,Dectin-1在B细胞中的功能知之甚少。为了确定Dectin-1在B细胞活化中的作用,我们首先研究小鼠B细胞是否表达Dectin-1,然后评估Dectin-1刺激对B细胞增殖和抗体产生的影响。小鼠B细胞表达编码TLR(包括Dectin-1)的mRNA,并且表面Dectin-1在C57 BL/6的B细胞中表达,而不是在BAL B/c株中表达。Dectin-1激动剂,热灭活的白色念珠菌(HKCA)和热灭活的酿酒酵母(HKSC),单独诱导B细胞增殖,但不产生抗体。有趣的是,HKSC,HKCA,和耗尽酵母聚糖(选择性Dectin-1激动剂)选择性增强LPS驱动的IgG 1生产。综上所述,这些结果表明,在真菌感染期间,β-葡聚糖刺激的Dectin-1可能与TLR 4协同作用,特异性增强小鼠B细胞的IgG 1产生。
Dectin-1, which specifically recognizes β-glucan of fungal cell walls, is a non-Toll-like receptor (TLR) pattern recognition receptor and a representative of C-type lectin receptors (CLRs). The importance of Dectin-1 in innate immune cells, such as dendritic cells and macrophages, has previously been well studied. However, the function of Dectin-1 in B cells is very poorly understood. To determine the role of Dectin-1 in B cell activation, we first investigated whether mouse B cells express Dectin-1 and then assessed the effect of Dectin-1 stimulation on B cell proliferation and antibody production. Mouse B cells express mRNAs encoding CLRs, including Dectin-1, and surface Dectin-1 was expressed in B cells of C57BL/6 rather than BALB/c strain. Dectin-1 agonists, heat-killed Candida albicans (HKCA) and heat-killed Saccharomyces cerevisiae (HKSC), alone induced B cell proliferation but not antibody production. Interestingly, HKSC, HKCA, and depleted zymosan (a selective Dectin-1 agonist) selectively enhanced LPS-driven IgG1 production. Taken together, these results suggest that, during fungal infection, β-glucan-stimulated Dectin-1 may cooperate with TLR4 to specifically enhance IgG1 production by mouse B cells.