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Abstract：
While antibiotics are intended to specifically target bacteria, most are known to affect host cell physiology. In addition, some antibiotic classes are reported as immunosuppressive for reasons that remain unclear. Here, we show that Linezolid, a ribosomal-targeting antibiotic (RAbo), effectively blocked the course of a T cell-mediated autoimmune disease. Linezolid and other RAbos were strong inhibitors of T helper-17 cell effector function in vitro, showing that this effect was independent of their antibiotic activity. Perturbing mitochondrial translation in differentiating T cells, either with RAbos or through the inhibition of mitochondrial elongation factor G1 (mEF-G1) progressively compromised the integrity of the electron transport chain. Ultimately, this led to deficient oxidative phosphorylation, diminishing nicotinamide adenine dinucleotide concentrations and impairing cytokine production in differentiating T cells. In accordance, mice lacking mEF-G1 in T cells were protected from experimental autoimmune encephalomyelitis, demonstrating that this pathway is crucial in maintaining T cell function and pathogenicity.
摘要：
虽然抗生素是专门针对细菌的，已知大多数影响宿主细胞生理学。此外,一些抗生素被报道为免疫抑制的原因尚不清楚.这里,我们展示了利奈唑胺，核糖体靶向抗生素（RAbo），有效阻断T细胞介导的自身免疫性疾病的进程。利奈唑胺和其他RAbos在体外是T辅助细胞17效应功能的强抑制剂，表明这种作用与它们的抗生素活性无关。在分化T细胞中扰动线粒体翻译，无论是用RAbos还是通过抑制线粒体延伸因子G1（mEF-G1）逐渐损害了电子传递链的完整性。最终,这导致氧化磷酸化不足，减少烟酰胺腺嘌呤二核苷酸浓度和削弱分化T细胞中细胞因子的产生。InAccording,在T细胞中缺乏mEF-G1的小鼠被保护免受实验性自身免疫性脑脊髓炎的影响，证明该途径在维持T细胞功能和致病性方面至关重要。
