Toll-like receptor 7 (TLR7) is an endosomal receptor, which recognizes single-stranded RNA from viruses. Its trafficking and activation is regulated by the endoplasmic reticulum chaperone UNC93B1 and lysosomal proteases. UNC93B1 also modulates major histocompatibility class II (MHCII) antigen presentation and deficiency in MHCII protein diminishes TLR9 signaling. These results indicate a link between proteins that regulate both innate and adaptive responses. Here we report that TLR7 resides in lysosomes and interacts with the MHCII-chaperone molecule, the invariant chain or CD74 in B cells. In the absence of CD74, TLR7 display both endoplasmic reticulum (ER) and lysosomal localization leading to an increase in pro-inflammatory cytokine production. Furthermore, TLR7 but not TLR9 stimulation is inefficient in boosting antigen presentation in Ii deficient cells. In contrast, in B cells lacking TLR7 or mutated for UNC93B1, which are enable to trigger TLR7 activation, antigen presentation is enhanced. This suggests that TLR7 signaling in B cells is controlled by Ii chain.

中文翻译：

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B 细胞中的 TLR7 运输和信号传导受 MHCII 相关不变链的调控。

Toll 样受体 7 (TLR7) 是一种内体受体，可识别病毒的单链 RNA。它的运输和激活受内质网伴侣 UNC93B1 和溶酶体蛋白酶的调控。UNC93B1 还调节主要组织相容性 II 类 (MHCII) 抗原呈递，MHCII 蛋白缺乏会减少 TLR9 信号。这些结果表明调节先天反应和适应性反应的蛋白质之间存在联系。在这里，我们报告 TLR7 存在于溶酶体中并与 MHCII 伴侣分子、不变链或 B 细胞中的 CD74 相互作用。在没有 CD74 的情况下，TLR7 显示出内质网 (ER) 和溶酶体定位，导致促炎细胞因子的产生增加。此外，TLR7 但不是 TLR9 刺激在促进 Ii 缺陷细胞中的抗原呈递方面效率低下。相比之下，在缺乏 TLR7 或 UNC93B1 突变的 B 细胞中，能够触发 TLR7 激活，抗原呈递增强。这表明 B 细胞中的 TLR7 信号传导受 Ii 链控制。