Selective utilization of Toll-like receptor and MyD88 signaling in B cells for enhancement of the antiviral germinal center response.

Selective utilization of Toll-like receptor and MyD88 signaling in B cells for enhancement of the antiviral germinal center response.
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DOI:
10.1016/j.immuni.2011.01.011
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发表时间:
2011-03-25
期刊:
影响因子:
32.4
通讯作者:
DeFranco AL
DeFranco AL
中科院分区:
医学1区
文献类型:
--
作者:
Hou B;Saudan P;Ott G;Wheeler ML;Ji M;Kuzmich L;Lee LM;Coffman RL;Bachmann MF;DeFranco AL

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Toll样受体(TLR)信号传导对T细胞依赖性(TD)抗体应答的贡献通过使用在单个细胞类型中缺乏TLR信号传导衔接子MyD88的小鼠来评估。当可溶性TLR9配体用作蛋白抗原的佐剂时,MyD 88在树突状细胞中是必需的,而在B细胞中不是必需的,以增强TD抗体应答,而不管抗原的固有免疫原性如何。相反,病毒样颗粒内含有的TLR9配体基本上增强了TD生殖中心IgG抗体应答,并且这种增强需要B细胞MyD 88。B细胞基于TLR配体的物理形式区分抗原的能力可能反映了促进强抗病毒抗体应答的适应。
The contribution of Toll-like receptor (TLR) signaling to T cell-dependent (TD) antibody responses was assessed by using mice lacking the TLR signaling adaptor MyD88 in individual cell types. When a soluble TLR9 ligand was used as adjuvant for a protein antigen, MyD88 was required in dendritic cells but not in B cells to enhance the TD antibody response, regardless of the inherent immunogenicity of the antigen. In contrast, a TLR9 ligand contained within a virus-like particle substantially augmented the TD germinal center IgG antibody response, and this augmentation required B cell MyD88. The ability of B cells to discriminate between antigens based the physical form of a TLR ligand likely reflects an adaptation to facilitate strong anti-viral antibody responses.
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