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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Potentiation of TLR9 responses for human naive B-cell growth through RP105 signaling.
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Potentiation of TLR9 responses for human naive B-cell growth through RP105 signaling.

机译：通过RP105信号转导对人类幼稚B细胞生长的TLR9反应的增强作用。

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摘要

Toll-like receptor 9 (TLR9) signals induce important pathways in the early defense against microbial pathogens. Although TLR9 signaling can activate memory B cells directly, efficient naive B cell responses seem to require additional, but as yet unidentified, signals. We explored the effects of RP105 (CD180) on CpG DNA-activated naive and memory B cells from normal controls and patients with common variable immunodeficiency (CVID). RP105 dramatically enhanced CpG DNA-induced proliferation/survival by naive B cells but not by memory B cells. This enhancement was mediated by TLR9 upregulation induced by RP105, leading to Akt activation and sustained NF-kappaB activation. CpG DNA-activated CVID B cells showed enhancement of proliferation/survival by RP105 and produced specific IgM antibody to Streptococcus pneumoniae polysaccharides in response to interleukin-21 stimulation. Thus, RP105 strongly affects expansion of the naive B-cell pool, and suggests that the putative RP105 ligand (s) upon cytokine stimulation facilitates antibody-mediated acute pathogen clearance.
机译：Toll样受体9（TLR9）信号诱导了早期防御微生物病原体的重要途径。尽管TLR9信号可以直接激活记忆B细胞，但有效的幼稚B细胞反应似乎需要其他但尚未确定的信号。我们探讨了RP105（CD180）对CpG DNA活化的天然和记忆B细胞的影响，这些细胞来自正常对照和具有常见可变免疫缺陷（CVID）的患者。 RP105显着增强了天真B细胞而非记忆B细胞对CpG DNA诱导的增殖/存活。这种增强是由RP105诱导的TLR9上调介导的，导致Akt激活和持续的NF-κB激活。 CpG DNA激活的CVID B细胞显示出通过RP105增强的增殖/存活，并响应白介素21刺激而产生了针对肺炎链球菌多糖的特异性IgM抗体。因此，RP105强烈影响幼稚B细胞池的扩展，并表明细胞因子刺激后推定的RP105配体可促进抗体介导的急性病原体清除。

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