Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (528 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Any of the infectious diseases of humans and other animals caused by species of mycobacterium tuberculosis.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Tuberculoses; Koch's Disease; Koch Disease; Kochs Disease; Mycobacterium tuberculosis Infection; Infection, Mycobacterium tuberculosis; Infections, Mycobacterium tuberculosis; Mycobacterium tuberculosis Infections.
Where it fits in the MeSH classification
- Broader topics
- Mycobacterium Infections
- Narrower topics
- Latent Tuberculosis; Tuberculoma; Tuberculosis Disease; Tuberculosis, Avian; Tuberculosis, Bovine; Tuberculosis, Extrapulmonary; Tuberculosis, Multidrug-Resistant; Tuberculosis, Pulmonary
- See also
- Antitubercular Agents; Tuberculin Test; Interferon-gamma Release Tests
Related concepts
- Humans
- Mycobacterium Tuberculosis
Research landscape
PubMed indexes 218,422 records tagged with the MeSH heading “Tuberculosis” (counts retrieved 2026-10-29). 26,588 of them (12.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 121,586 records.
Reviews account for 16,079 records (7.4%) and meta-analyses for 1,516. Randomized controlled trials number 1,823 (0.8%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 121,586 |
| 2000-2009 | 28,659 |
| 2010-2019 | 41,589 |
| 2020 onward | 26,588 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 16,079 | 7.4% |
| Meta-analyses | 1,516 | 0.7% |
| Randomized controlled trials | 1,823 | 0.8% |
Method: PubMed query "Tuberculosis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in infectious diseases
Infectious disease evidence combines microbiology, epidemiology and clinical trials. Laboratory studies identify pathogens and how they cause harm; surveillance and outbreak investigations describe who is affected and how infection spreads; trials establish whether treatments and vaccines work. Results depend on place and time, because pathogens evolve and resistance patterns and population immunity change. Check when and where the data were collected, how cases were defined and how up to date the evidence is.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42600620 · DOI · PMC13528601 |
| Inflammatory biomarkers of asymptomatic and symptomatic tuberculosis | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42649201 · DOI · PMC13518882 |
| Therapeutic remodeling of the tuberculosis granuloma with 1-methyl-D-tryptophan enhances CD8+ T cell-macrophage interactions | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42579482 · DOI · PMC13486567 |
Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Mycobacterium tuberculosis (Mtb) causes over one million deaths annually, but most infected individuals never exhibit symptoms.
- Closing excerpt
- Our results demonstrate that strong and sustained type I IFN responses specifically and cell intrinsically impair responsiveness to IFNγ to cause susceptibility to Mtb.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (158 words)
Mycobacterium tuberculosis (Mtb) causes over one million deaths annually, but most infected individuals never exhibit symptoms. Type I interferons (IFNs) have emerged as a major factor driving susceptibility to Mtb, but how type I IFNs impair immunity to Mtb is a key unresolved question. Here, we show that an early effect of type I IFN during Mtb infection is the cell-intrinsic impairment of IFNγ signaling. IFNγ signaling is selectively impaired in the subset of infected macrophages experiencing high and sustained levels of type I IFN signaling. Genetic elimination of regulated stimulator of interferon via stabilization of transcript (RESIST), a recently described positive regulator of type I IFN production, specifically eliminates the high and sustained type I IFN response, fully restores IFNγ signaling, and rescues susceptibility to Mtb without affecting basal type I IFN responses. Our results demonstrate that strong and sustained type I IFN responses specifically and cell intrinsically impair responsiveness to IFNγ to cause susceptibility to Mtb.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42600620 · DOI · PMC13528601
Inflammatory biomarkers of asymptomatic and symptomatic tuberculosis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- A large proportion of individuals with tuberculosis (TB) are asymptomatic.
- Closing excerpt
- However, diagnostic performance of transcriptomic and proteomic markers is weaker for asymptomatic TB than symptomatic TB, suggesting that policy development for community-based, asymptomatic TB screening should not adopt biomarkers developed for symptomatic TB triage without further optimization.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
A large proportion of individuals with tuberculosis (TB) are asymptomatic. The biological and inflammatory underpinnings of asymptomatic TB are unknown and may differ from symptomatic TB. We characterise blood transcriptomic and proteomic profiles in South African community screening vs. health facility-based triage cohorts. Asymptomatic TB shares core transcriptomic and proteomic features with symptomatic TB, including upregulation of innate, interferon and inflammatory pathways and downregulation of T and B cell pathways. Integration of transcriptomic and proteomic data from asymptomatic TB individuals identifies two distinct sub-clusters characterized by higher or lower bacterial burden, blood IFN-γ responses, BMI, and chest radiographic abnormalities, suggesting different disease severity. We identify a new blood transcriptomic signature of asymptomatic TB. However, diagnostic performance of transcriptomic and proteomic markers is weaker for asymptomatic TB than symptomatic TB, suggesting that policy development for community-based, asymptomatic TB screening should not adopt biomarkers developed for symptomatic TB triage without further optimization.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42649201 · DOI · PMC13518882
Therapeutic remodeling of the tuberculosis granuloma with 1-methyl-D-tryptophan enhances CD8+ T cell-macrophage interactions [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Granulomas, the hallmark of tuberculosis (TB) disease, can both restrict Mycobacterium tuberculosis (Mtb) dissemination and impede its clearance.
- Closing excerpt
- Our results demonstrate that: i) effective intragranulomatous Mtb control is associated with the close spatial proximity between CD8+ T cells and macrophages, a feature less abundant in uncontrolled pulmonary TB; ii) IDO1 induction blocks CD8+ T cell infiltration and reduces T cell activation and proliferation; and iii) therapeutic strategies, including D-1MT, that improve intragranulomatous killing hold strong translational potential.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (220 words)
Granulomas, the hallmark of tuberculosis (TB) disease, can both restrict Mycobacterium tuberculosis (Mtb) dissemination and impede its clearance. Recent studies indicate that indoleamine 2,3-dioxygenase (IDO1), an immunosuppressive metabolic enzyme, limits infiltration of activated T cells and can contribute to TB disease progression. Treatment with 1-methyl-D-tryptophan (D-1MT), a small molecule inhibitor that restores mTOR signaling, has been shown to reduce IDO1 activity and improve immune responses in Mtb-infected rhesus macaques. Here, we investigated the impact of D-1MT treatment on TB granuloma architecture using 30-plex high-dimensional issue imaging in rhesus macaques. By spatially mapping 13 distinct cell populations, we found D-1MT treatment corresponded with significantly increased infiltration CD8+ T cells into granulomas compared to untreated controls. Notably, these CD8+ T cells expressed markers of cell proliferation and cytotoxicity. D-1MT enhanced CD8+ T cell infiltration throughout the granuloma, with particularly pronounced effects in the myeloid core, where we observed significantly enhanced spatial interactions between macrophages and CD8+ T cells, but not CD4+ T cells. Our results demonstrate that: i) effective intragranulomatous Mtb control is associated with the close spatial proximity between CD8+ T cells and macrophages, a feature less abundant in uncontrolled pulmonary TB; ii) IDO1 induction blocks CD8+ T cell infiltration and reduces T cell activation and proliferation; and iii) therapeutic strategies, including D-1MT, that improve intragranulomatous killing hold strong translational potential.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42579482 · DOI · PMC13486567
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Infant BCG vaccination and risk of pulmonary and extrapulmonary tuberculosis throughout the life course: a systematic review and individual participant data meta-analysis [4]
- Research article Global prevalence of drug-resistant tuberculosis: a systematic review and meta-analysis [5]
- Research article Post-tuberculosis lung impairment: systematic review and meta-analysis of spirometry data from 14 621 people [6]
- Research article The natural history of untreated pulmonary tuberculosis in adults: a systematic review and meta-analysis [7]
- Research article Global morbidity and mortality of central nervous system tuberculosis: a systematic review and meta-analysis [8]
- Research article Prevalence of subclinical pulmonary tuberculosis in adults in community settings: an individual participant data meta-analysis [9]
References
- Fattinger SA, Parisi B, Chavez RA, Fairgrieve MR, Lee OV, Witt KC, et al.. Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility. . 2026. PMID 42600620 · DOI · PMC13528601
- Awany D, Ariefdien DT, Mendelsohn SC, Rozot V, Mulenga H, Nyangu S, et al.. Inflammatory biomarkers of asymptomatic and symptomatic tuberculosis. . 2026. PMID 42649201 · DOI · PMC13518882
- McCaffrey EF, Delmastro AC, Singh B, Devi A, Munson CW, Priyanka, et al.. Therapeutic remodeling of the tuberculosis granuloma with 1-methyl-D-tryptophan enhances CD8+ T cell-macrophage interactions. . 2026. PMID 42579482 · DOI · PMC13486567
- Martinez L, Cords O, Liu Q, Acuna-Villaorduna C, Bonnet M, Fox GJ, et al.. Infant BCG vaccination and risk of pulmonary and extrapulmonary tuberculosis throughout the life course: a systematic review and individual participant data meta-analysis. Lancet Glob Health. 2022. PMID 35961354 · DOI · PMC10406427
- Salari N, Kanjoori AH, Hosseinian-Far A, Hasheminezhad R, Mansouri K, Mohammadi M. Global prevalence of drug-resistant tuberculosis: a systematic review and meta-analysis. Infect Dis Poverty. 2023. PMID 37231463 · DOI · PMC10210422
- Ivanova O, Hoffmann VS, Lange C, Hoelscher M, Rachow A. Post-tuberculosis lung impairment: systematic review and meta-analysis of spirometry data from 14 621 people. Eur Respir Rev. 2023. PMID 37076175 · DOI · PMC10113954
- Sossen B, Richards AS, Heinsohn T, Frascella B, Balzarini F, Oradini-Alacreu A, et al.. The natural history of untreated pulmonary tuberculosis in adults: a systematic review and meta-analysis. Lancet Respir Med. 2023. PMID 36966795 · DOI
- Navarro-Flores A, Fernandez-Chinguel JE, Pacheco-Barrios N, Soriano-Moreno DR, Pacheco-Barrios K. Global morbidity and mortality of central nervous system tuberculosis: a systematic review and meta-analysis. J Neurol. 2022. PMID 35288778 · DOI · PMC8920747
- Stuck L, Klinkenberg E, Abdelgadir Ali N, Basheir Abukaraig EA, Adusi-Poku Y, Alebachew Wagaw Z, et al.. Prevalence of subclinical pulmonary tuberculosis in adults in community settings: an individual participant data meta-analysis. Lancet Infect Dis. 2024. PMID 38490237 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.