A role for Toll-like receptors in acquired immunity: up-regulation of TLR9 by BCR triggering in naive B cells and constitutive expression in memory B cells
A role for Toll-like receptors in acquired immunity: up-regulation of TLR9 by BCR triggering in naive B cells and constitutive expression in memory B cells
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DOI：
10.1182/blood-2002-11-3569
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发表时间：
2003-06-01
期刊：
影响因子：
20.3
通讯作者：
Lanzavecchia, A
中科院分区：
文献类型：
--
作者：
Bernasconi, NL;Onai, N;Lanzavecchia, A
Toll样受体（TLR）是触发先天免疫的模式识别受体。在这项研究中，我们研究了10个TLR在人类幼稚和记忆中的表达。B细胞亚群我们报道了在人类幼稚B细胞中，大多数TLR以低至不可检测的水平表达，但TLR 6和TLR 10的表达在B细胞受体（BCR）触发后被迅速诱导。相反，记忆5细胞以组成性高水平表达几种TLR。TLR9的差异表达与其激动剂CpG DNA的反应性相关。因此，人类记忆B细胞增殖并分化为免疫球蛋白（IG）分泌细胞，以响应CpG，而幼稚B只有在同时通过BCR触发时才这样做。BCR诱导的人幼稚B细胞中TLR的表达阻止了初次应答中的多克隆活化，因为它限制了对抗原特异性B细胞的刺激。相反，TLR在记忆B细胞中的组成型表达允许整个记忆池的多克隆活化。因此，在人B细胞中，TLR位于BCR的下游，并在初级应答中发挥作用。在记忆阶段。(C)2003年，美国血液学会。
Toll-like receptors (TLRs) are pattern recognition receptors that trigger innate immunity. In this study we investigated the expression of 10 TLRs in human naive and memory. B-cell subsets. We report that in human naive B cells-most TLRs are expressed at low to undetectable levels, but the expression of TLR6 and TLR10 is rapidly induced following B-cell-receptor (BCR) triggering. In contrast, memory 5 cells express several TLRs at constitutively high levels. The differential expression of TLR9 correlates with responsiveness to its agonist, CpG DNA. Thus, human memory B cells proliferate and differentiate to immunoglobulin (Ig)-secreting cells in response to CpG, while naive B do so only if simultaneously triggered through the BCR. The BCR-induced expression of TLRs in human naive B cells prevents polyclonal activation in a primary response, because it restricts stimulation to antigen-specific B c ells. In contrast, the constitutive expression of TLRs in memory B cells allows polyclonal activation of the entire memory pool. Thus, in human B cells TLRs are downstream of BCR and play a role both in the primary response. and in the memory phase. (C) 2003 by The American Society of Hematology.