The bacterium Staphylococcus aureus is an important cause of the life-threatening condition toxic shock syndrome in humans. Bacterial toxins known as superantigens (SAgs) generate this illness by acting as broad activators of a substantial fraction of all T lymphocytes, bypassing the normally highly stringent T-cell receptor antigen specificity to cause a systemic inflammatory cytokine storm in the host. In a new study, Shaler et al. found that immune cells called mucosa-associated invariant T (MAIT) cells make an unexpectedly large contribution to the SAg response in a largely T-cell receptor–independent, cytokine-driven manner. Subsequent to such activation, the MAIT cells remain unresponsive to stimulation with bacterial antigen. Thus, S. aureus hijacks MAIT cells in the cytokine storm and leaves them functionally impaired. This work provides new insight into the role of MAIT cells in antibacterial immunity and opens new avenues of investigation to understand and possibly treat bacterial toxic shock and sepsis.

金黄色葡萄球菌细菌是威胁人类生命的中毒性休克综合症的重要原因。被称为超抗原（SAgs）的细菌毒素通过充当所有T淋巴细胞中相当大部分的广泛激活剂而绕过通常高度严格的T细胞受体抗原特异性，从而在宿主中引起全身性炎性细胞因子风暴，从而导致这种疾病。在一项新的研究中，Shaler等人。发现被称为粘膜相关不变T（MAIT）的免疫细胞以很大程度上独立于T细胞受体的细胞因子驱动方式，对SAg反应做出了出乎意料的巨大贡献。在这种活化之后，MAIT细胞保持对细菌抗原刺激无反应。因此，S。金黄色在细胞因子风暴中劫持了MAIT细胞，并使它们的功能受损。这项工作为MAIT细胞在抗菌免疫中的作用提供了新的见识，并开辟了新的研究途径，以了解并可能治疗细菌中毒性休克和败血症。