<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Collins JM</submitter><funding>National Institute of Allergy and Infectious Diseases</funding><funding>NIAID NIH HHS</funding><funding>FIC NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIH Fogarty International Center</funding><funding>NIH HHS</funding><pagination>235-243</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12573232</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>233(2)</volume><pubmed_abstract>Greater understanding of the role of tryptophan metabolism in the immune response to tuberculosis (TB) has provided promising avenues to explore new diagnostic and therapeutic modalities. Animal and human studies have demonstrated that host indoleamine 2,3-dioxygenase 1 (IDO1) is upregulated in response to infection with Mycobacterium tuberculosis, resulting in increased tryptophan metabolism to kynurenine. In TB disease, this is evidenced by elevation of the plasma kynurenine to tryptophan ratio, which is reversed with effective TB treatment, thus showing utility as a potential diagnostic and therapeutic biomarker. Kynurenine and downstream metabolites promote an immunosuppressive microenvironment in TB granulomas, which may facilitate immune evasion. IDO inhibition in nonhuman primates h</pubmed_abstract><journal>The Journal of infectious diseases</journal><pubmed_title>Targeting Tryptophan Metabolism for Tuberculosis Biomarkers and Host-Directed Therapy.</pubmed_title><pmcid>PMC12573232</pmcid><funding_grant_id>P30AI168386</funding_grant_id><funding_grant_id>R01AI173946</funding_grant_id><funding_grant_id>D43 TW007124</funding_grant_id><funding_grant_id>K23AI144040</funding_grant_id><funding_grant_id>K24 AI190403</funding_grant_id><funding_grant_id>P30 AI168386</funding_grant_id><funding_grant_id>D43TW007124</funding_grant_id><funding_grant_id>R01 AI173946</funding_grant_id><funding_grant_id>R21AI178324</funding_grant_id><funding_grant_id>R21 AI178324</funding_grant_id><funding_grant_id>K23 AI144040</funding_grant_id><funding_grant_id>R01 AI182244</funding_grant_id><funding_grant_id>R01AI182244</funding_grant_id><pubmed_authors>Collins JM</pubmed_authors><pubmed_authors>Tukvadze N</pubmed_authors><pubmed_authors>Kempker RR</pubmed_authors></additional><is_claimable>false</is_claimable><name>Targeting Tryptophan Metabolism for Tuberculosis Biomarkers and Host-Directed Therapy.</name><description>Greater understanding of the role of tryptophan metabolism in the immune response to tuberculosis (TB) has provided promising avenues to explore new diagnostic and therapeutic modalities. Animal and human studies have demonstrated that host indoleamine 2,3-dioxygenase 1 (IDO1) is upregulated in response to infection with Mycobacterium tuberculosis, resulting in increased tryptophan metabolism to kynurenine. In TB disease, this is evidenced by elevation of the plasma kynurenine to tryptophan ratio, which is reversed with effective TB treatment, thus showing utility as a potential diagnostic and therapeutic biomarker. Kynurenine and downstream metabolites promote an immunosuppressive microenvironment in TB granulomas, which may facilitate immune evasion. IDO inhibition in nonhuman primates h</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Feb</publication><modification>2026-07-09T11:11:02.734Z</modification><creation>2026-07-09T10:42:03.482Z</creation></dates><accession>S-EPMC12573232</accession><cross_references><pubmed>41037490</pubmed><doi>10.1093/infdis/jiaf510</doi></cross_references></HashMap>