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IDO inhibits the function of immune cells through a specific L-Trp depletion pathway, where L-Trp depletion by IDO leads to its dissociation with L-Trp tRNA, thus activating general control non-derepressible 2 (GCN2) due to the presence of its allosteric regulatory site which senses free tRNAs (47, 48)

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Similarly, beta-lactams and fluoroquinolones, the first-line antibiotics, have been found to play a significant role in the AMR burden globally 33,34

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