Type I IFN enhances follicular B cell contribution to the T cell-independent antibody response.
Type I IFN enhances follicular B cell contribution to the T cell-independent antibody response.
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DOI：
10.1084/jem.20092695
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发表时间：
2010-07-05
期刊：
影响因子：
--
通讯作者：
Torres RM
中科院分区：
文献类型：
--
作者：
Swanson CL;Wilson TJ;Strauch P;Colonna M;Pelanda R;Torres RM
针对病毒和包膜细菌的体液免疫由T细胞非依赖性2型(TI-2)抗体反应组成，其特征是边缘带和B1 B细胞快速产生抗体。我们证明Toll样受体(TLR)配体影响TI-2抗体反应不仅是通过提高整体反应幅度，而且是通过使这种反应偏向以免疫球蛋白同型为主的反应。重要的是，TLR配体通过诱导I型干扰素(IFN)促进这种反应，I型干扰素继而引发快速而大量的抗原特异性IgG2c，主要来自FO(滤泡)B细胞。此外，我们还表明，虽然IgG2c抗体反应需要B细胞自主的干扰素-α受体信号，但它不依赖于B细胞固有的TLR信号。因此，天然信号有能力通过促进FO B细胞的参与来增强TI-2抗体的应答，然后FO B细胞产生有效的抗病原体抗体。
Humoral immunity to viruses and encapsulated bacteria is comprised of T cell–independent type 2 (TI-2) antibody responses that are characterized by rapid antibody production by marginal zone and B1 B cells. We demonstrate that toll-like receptor (TLR) ligands influence the TI-2 antibody response not only by enhancing the overall magnitude but also by skewing this response to one that is dominated by IgG isotypes. Importantly, TLR ligands facilitate this response by inducing type I interferon (IFN), which in turn elicits rapid and significant amounts of antigen-specific IgG2c predominantly from FO (follicular) B cells. Furthermore, we show that although the IgG2c antibody response requires B cell–autonomous IFN-α receptor signaling, it is independent of B cell–intrinsic TLR signaling. Thus, innate signals have the capacity to enhance TI-2 antibody responses by promoting participation of FO B cells, which then elaborate effective IgG anti-pathogen antibodies.
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