title: Trp'ing tuberculosis.
abstract: IFN-γ-activated macrophages attempt to limit pathogen growth through tryptophan starvation. Zhang et al. demonstrate that Mycobacterium tuberculosis responds to this threat by synthesizing its own tryptophan. Genetic and chemical inhibition of this pathway reduces mycobacterial survival, revealing a new immune-dependent drug target for tuberculosis.
authors: Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA. Electronic address: dgr8@cornell.edu.
authors: David G
authors: DG
authors: Russell
mesh_terms: D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D006801:Humans; D009169:Mycobacterium tuberculosis / Q000378:metabolism*; D014364:Tryptophan / Q000096:biosynthesis*; D014376:Tuberculosis / Q000276:immunology* / Q000382:microbiology*
chemical_list: D014364:Tryptophan