The DOI matches its Crossref record; 54 of the 55 references it cites were found in a registry or an index.
M. tuberculosis Induces Potent Activation of IDO-1, but This Is Not Essential for the Immunological Control of Infection
Open accessAbstract
Indoleamine 2,3-dioxygenesae-1 (IDO-1) catalyses the initial, rate-limiting step in tryptophan metabolism, thereby regulating tryptophan availability and the formation of downstream metabolites, including picolinic and quinolinic acid. We found that Mycobacterium tuberculosis infection induced marked upregulation of IDO-1 expression in both human and murine macrophages in vitro and in the lungs of mice following aerosol challenge with M. tuberculosis. The absence of IDO-1 in dendritic cells enhanced the activation of mycobacteria-specific T cells in vitro. Interestingly, IDO-1-deficiency during M. tuberculosis infection in mice was not associated with altered mycobacteria-specific T cell responses in vivo. The bacterial burden of infected organs, pulmonary inflammatory responses, and survival were also comparable in M. tuberculosis-infected IDO-1 deficient and wild type animals. Tryptophan is metabolised into either picolinic acid or quinolinic acid, but only picolinic acid inhibited the growth of M. tuberculosis in vitro. By contrast macrophages infected with pathogenic mycobacteria, produced quinolinic, rather than picolinic acid, which did not reduce M. tuberculosis growth in vitro. Therefore, although M. tuberculosis induces robust expression of IDO-1 and activation of tryptophan metabolism, IDO-1-deficiency fails to impact on the immune control and the outcome of the infection in the mouse model of tuberculosis.
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“However, in the setting of M. tuberculosis infection, IDO activation appears to be ineffective in controlling the infection.”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [96]
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“IDO deficient mice were able to control M. tuberculosis infection as good as wildtype animals and lack of IDO did not affect mycobacterial specific T-cell responses (96).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [96]
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“Tryptophan is essential for M. tuberculosis growth, however, IDO deficient mice were able to control M. tuberculosis infection as good as wildtype animals and lack of IDO did not affect mycobacterial specific T-cell responses (96).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [96]
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Cites
Prevention of Allogeneic Fetal Rejection by Tryptophan Catabolism
Munn, D. H., Zhou, M., Attwood, J. T., Bondarev, I. E., Conway, S. J., Marshall, B., Brown, C. C., & Mellor, A. L. (1998) · Science · doi:10.1126/science.281.5380.1191 · Cited by 2,589
An essential role for interferon gamma in resistance to Mycobacterium tuberculosis infection.
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Disseminated tuberculosis in interferon gamma gene-disrupted mice.
Cooper, A. M., Dalton, D. K., Stewart, T. A., Griffin, J. P., Russell, D. G., & Orme, I. M. (1993) · The Journal of Experimental Medicine · doi:10.1084/jem.178.6.2243 · Cited by 1,987
Inhibition of T Cell Proliferation by Macrophage Tryptophan Catabolism
Munn, D. H., Shafizadeh, E., Attwood, J. T., Bondarev, I. E., Pashine, A., & Mellor, A. L. (1999) · The Journal of Experimental Medicine · doi:10.1084/jem.189.9.1363 · Cited by 1,640
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Potential Regulatory Function of Human Dendritic Cells Expressing Indoleamine 2,3-Dioxygenase
Munn, D. H., Sharma, M. D., Lee, J. R., Jhaver, K. G., Johnson, T. S., Keskin, D. B., Marshall, B., Chandler, P., Antonia, S. J., Burgess, R. E., et al. (2002) · Science · doi:10.1126/science.1073514 · Cited by 1,028
Genetic Dissection of Immunity to Mycobacteria: The Human Model
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Monitoring tryptophan metabolism in chronic immune activation
Schröcksnadel, K., Wirleitner, B., Winkler, C., & Fuchs, D. (2006) · Clinica Chimica Acta · doi:10.1016/j.cca.2005.06.013 · Cited by 551 · cited 1×
“IDO-2 remained unchanged during Plasmodium berghei ANKA infection [46] and TDO activity has also not been associated with immunerelated tryptophan metabolism [47].”
BackgroundFavre, D., Mold, J. E., Hunt, P. W., Kanwar, B., Loke, P., Seu, L., Barbour, J. D., Lowe, M. M., Jayawardene, A., Aweeka, F. T., et al. (2010) · Science Translational Medicine · doi:10.1126/scitranslmed.3000632 · Cited by 545
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Items 101–105 of 105
Doltrário, A. B., Lee, M. H., Broll, S., Dupnik, K. M., Rouzier, V., Sévère, P., Dorvil, N., Pape, J. W., Koenig, S. P., Fitzgerald, D. W., et al. (2025) · medRxiv · doi:10.1101/2025.08.21.25334178
Dissecting Tuberculosis Through Transcriptomic Studies
Rodrigues, R. F., Rosada, R. S., Malardo, T., Rios, W. M., & Silva, C. L. (2014) · Springer eBooks · doi:10.1007/978-3-319-11985-4_15
张晓娟, Liu, Y., Hou, Y., & Niu, H. (2026) · MedComm · doi:10.1002/mco2.70884
Stasiak, P., Kraśnik, K., Biskupski, M., Tarka, A., Flis, M., & Urbańska, E. M. (2026) · Life · doi:10.3390/life16081350
Core Metabolic Pathways and Their Metabolomic Signature in Pathogens
Doltrário, A. B., Rosenn, E. H., Li, S., Sunchu, B., Padmanarayana, M., Kumari, J., & Soni, V. (2026) · Springer eBooks · doi:10.1007/978-3-032-30306-6_2
Metadata
- Authors
- Blumenthal, A., Nagalingam, G., Huch, J. H., Walker, L., Guillemin, G. J., Smythe, G. A., Ehrt, S., Britton, W. J., & Saunders, B. M.
- Affiliations
- The University of Queensland (AU)
- Centenary Institute (AU)
- UNSW Sydney (AU)
- Cornell University (US)
- The University of Sydney (AU)
- Corresponding author
- Blumenthal, Antje
- Saunders, Bernadette M.
- ORCID
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-05-23
- Volume
- 7
- Issue
- 5
- Pages
- e37314
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3359358
- OpenAlex
- W2025969665
- Cited by
- 105
- References
- 55
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 7 · 2023: 7 · 2022: 6 · 2021: 10 · 2020: 14 · 2019: 7 · 2018: 10 · 2017: 7 · 2016: 6 · 2015: 11 · 2014: 6 · 2013: 5 · 2012: 2
- FWCI
- 5.30
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- UTS ePRESS (University of Technology Sydney) (submittedVersion)
- Funders
- National Institutes of Health
- Medical Research Council
- National Health and Medical Research Council
- National Heart, Lung, and Blood Institute (R01HL068525, HL68525)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Health Sciences › Medicine › Infectious Diseases › Infectious Diseases and Tuberculosis
- Keywords
- Mycobacterium tuberculosis, IDO1, tryptophan metabolism, tryptophan catabolism, picolinic acid, quinolinic acid, macrophages, dendritic cells, tuberculosis immunology, bacterial growth inhibition
- MeSH terms
- Animals, Female, Humans, Immunohistochemistry, Lung, Macrophages, Mice, Inbred C57BL, Mycobacterium tuberculosis, Picolinic Acids, T-Lymphocytes, Tryptophan, Tuberculosis, Blotting, Western, DNA Primers, Mice, Knockout, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Microarray Analysis, Indoleamine-Pyrrole 2,3,-Dioxygenase, Mice, Kaplan-Meier Estimate, Real-Time Polymerase Chain Reaction
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