Mucosal-associated invariant T (MAIT) cells are innate T lymphocytes activated by bacteria that produce vitamin B2 metabolites. Mouse models of infection have demonstrated a role for MAIT cells in antimicrobial defense. However, proposed protective roles of MAIT cells in human infections remain unproven and clinical conditions associated with selective absence of MAIT cells have not been identified. We report that typhoidal and nontyphoidal Salmonella enterica strains activate MAIT cells. However, S. Typhimurium sequence type 313 (ST313) lineage 2 strains, which are responsible for the burden of multidrug-resistant nontyphoidal invasive disease in Africa, escape MAIT cell recognition through overexpression of ribB. This bacterial gene encodes the 4-dihydroxy-2-butanone-4-phosphate synthase enzyme of the riboflavin biosynthetic pathway. The MAIT cell-specific phenotype did not extend to other innate lymphocytes. We propose that ribB overexpression is an evolved trait that facilitates evasion from immune recognition by MAIT cells and contributes to the invasive pathogenesis of S. Typhimurium ST313 lineage 2.

黏膜相关不变 T (MAIT) 细胞是由产生维生素 B2 代谢物的细菌激活的先天 T 淋巴细胞。感染的小鼠模型已经证明 MAIT 细胞在抗菌防御中的作用。然而，提出的 MAIT 细胞在人类感染中的保护作用仍未得到证实，并且与 MAIT 细胞选择性缺失相关的临床状况尚未确定。我们报告伤寒和非伤寒肠沙门氏菌菌株激活 MAIT 细胞。然而，鼠伤寒沙门氏菌序列类型 313 (ST313) 谱系 2 菌株，负责非洲耐多药非伤寒侵袭性疾病的负担，通过 ribB 的过表达逃避 MAIT 细胞识别. 该细菌基因编码核黄素生物合成途径的 4-二羟基-2-丁酮-4-磷酸合酶。MAIT 细胞特异性表型未扩展到其他先天淋巴细胞。我们提出ribB过表达是一种进化特征，它有助于逃避 MAIT 细胞的免疫识别，并有助于S. Typhimurium ST313 谱系 2 的侵袭性发病机制。