The gut mounts secretory immunoglobulin A (SIgA) responses to commensal bacteria through nonredundant T cell–dependent (TD) and T cell–independent (TI) pathways that promote the establishment of mutualistic host-microbiota interactions. SIgAs from the TD pathway target penetrant bacteria, and their induction requires engagement of CD40 on B cells by CD40 ligand on T follicular helper cells. In contrast, SIgAs from the TI pathway bind a larger spectrum of bacteria, but the mechanism underpinning their production remains elusive. Here, we show that the intestinal TI pathway required CD40-independent B cell–activating signals from TACI, a receptor for the innate CD40 ligand–like factors BAFF and APRIL. TACI-induced SIgA responses targeted a fraction of the gut microbiota without shaping its overall composition. Of note, TACI was dispensable for TD induction of IgA in gut-associated lymphoid organs. Thus, BAFF/APRIL signals acting on TACI orchestrate commensal bacteria–specific SIgA responses through an intestinal TI program.

肠道通过非冗余 T 细胞依赖性 (TD) 和 T 细胞非依赖性 (TI) 途径对共生细菌产生分泌性免疫球蛋白 A (SIgA) 反应，促进宿主-微生物群相互作用的建立。来自 TD 途径的 SIgAs 靶向渗透细菌，它们的诱导需要 T 滤泡辅助细胞上的 CD40 配体与 B 细胞上的 CD40 结合。相比之下，来自 TI 途径的 SIgAs 可以结合更广泛的细菌，但其产生的机制仍然难以捉摸。在这里，我们表明肠道 TI 途径需要来自 TACI 的 CD40 独立 B 细胞激活信号，TACI 是先天 CD40 配体样因子 BAFF 和 APRIL 的受体。TACI 诱导的 SIgA 反应针对肠道微生物群的一部分，但不改变其整体组成。值得注意的是，对于肠道相关淋巴器官中 IgA 的 TD 诱导，TACI 是可有可无的。因此，作用于 TACI 的 BAFF/APRIL 信号通过肠道 TI 程序协调共生细菌特异性 SIgA 反应。