Correction: The intracellular pathogen escapes from adaptive immunity by metabolic adaptation.

This study shows that this metabolic adaptation allows the intracellular bacterial pathogen to escape recognition by the host adaptive immunity.

The intracellular pathogen escapes from adaptive immunity by metabolic adaptation.

Intracellular pathogens lose many metabolic genes during their evolution from free-living bacteria, but the pathogenic consequences of their altered metabolic programs on host immunity are poorly understood. Here, we show that a pathogenic strain of (FT) has five amino acid substitutions in RibD, a converting enzyme of the riboflavin synthetic pathway responsible for generating metabolites recognized by mucosal-associated invariant T (MAIT) cells. Metabolites from a free-living strain, (FN), activated MAIT cells in a T-cell receptor (TCR)-dependent manner, whereas introduction of FT-type to the free-living strain was sufficient to attenuate this activation in both human and mouse MAIT cells.