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Publication

Ribosome-Targeting Antibiotics Impair T Cell Effector Function and Ameliorate Autoimmunity by Blocking Mitochondrial Protein Synthesis.

Immunity | 2021

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.

Pubmed ID: 33238133 RIS Download

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Associated grants

Agency: NIAID NIH HHS, United States
Id: P01 AI056299
Agency: NCI NIH HHS, United States
Id: P01 CA065493
Agency: NHLBI NIH HHS, United States
Id: R01 HL118979
Agency: NIAID NIH HHS, United States
Id: R37 AI034495
Agency: NHLBI NIH HHS, United States
Id: R01 HL155114
Agency: NHLBI NIH HHS, United States
Id: R01 HL056067
Agency: Wellcome Trust, United Kingdom

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