Organisms use l-amino acids (l-aa) for most physiological processes. Unlike other organisms, bacteria chiral-convert l-aa to d-configurations as essential components of their cell walls and as signaling molecules in their ecosystems. Mammals recognize microbe-associated molecules to initiate immune responses, but roles of bacterial d-amino acids (d-aa) in mammalian immune systems remain largely unknown. Here, we report that amino acid chirality balanced by bacteria-mammal cross-talk modulates intestinal B cell fate and immunoglobulin A (IgA) production. Bacterial d-aa stimulate M1 macrophages and promote survival of intestinal naïve B cells. Mammalian intestinal d-aa catabolism limits the number of B cells and restricts growth of symbiotic bacteria that activate T cell–dependent IgA class switching of the B cells. Loss of d-aa catabolism results in excessive IgA production and dysbiosis with altered IgA coating on bacteria. Thus, chiral conversion of amino acids is linked to bacterial recognition by mammals to control symbiosis with bacteria.

生物体在大多数生理过程中使用l-氨基酸 ( l -aa)。与其他生物体不同，细菌手性将l - aa 转换为d-构型，作为其细胞壁的重要组成部分和生态系统中的信号分子。哺乳动物识别微生物相关分子以启动免疫反应，但细菌d-氨基酸 ( d - aa) 在哺乳动物免疫系统中的作用仍然很大程度上未知。在这里，我们报告了由细菌-哺乳动物串扰平衡的氨基酸手性调节肠道 B 细胞命运和免疫球蛋白 A (IgA) 的产生。细菌_-aa 刺激 M1 巨噬细胞并促进肠道幼稚 B 细胞的存活。哺乳动物肠道d -aa 分解代谢限制了 B 细胞的数量并限制了共生细菌的生长，这些细菌激活了 B 细胞的依赖于 T 细胞的 IgA 类别转换。d -aa 分解代谢的丧失导致过度的 IgA 产生和菌群失调，细菌上的 IgA 涂层发生改变。因此，氨基酸的手性转化与哺乳动物的细菌识别有关，以控制与细菌的共生。