ArticleThe Journal of experimental medicine2001
Alphabeta T cell receptor-positive cells and interferon-gamma, but not inducible nitric oxide synthase, are critical for granuloma necrosis in a mouse model of mycobacteria-induced pulmonary immunopathology.
Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 109 citations in OpenAlex.
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- SP110b Controls Host Immunity and Susceptibility to Tuberculosis.American journal of respiratory and critical care medicine · 2017Article
- Animal Models for Tuberculosis in Translational and Precision Medicine.Frontiers in microbiology · 2017Review
- Molecular diagnosis: Implications for ophthalmology.Progress in retinal and eye research · 2016Review
- Lack of the Transcription Factor Hypoxia-Inducible Factor 1α (HIF-1α) in Macrophages Accelerates the Necrosis of Mycobacterium avium-Induced Granulomas.Infection and immunity · 2015Article
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- Orchestration of pulmonary T cell immunity during Mycobacterium tuberculosis infection: immunity interruptus.Seminars in immunology · 2014Review
- Tuberculosis, pulmonary cavitation, and matrix metalloproteinases.American journal of respiratory and critical care medicine · 2014Article
- Systemic and mucosal immune reactivity upon Mycobacterium avium ssp. paratuberculosis infection in mice.PloS one · 2014Article
- CD4+ cell-dependent granuloma formation in humanized mice infected with mycobacteria.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- IL-10 inhibits mature fibrotic granuloma formation during Mycobacterium tuberculosis infection.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- IL-22 is mainly produced by IFNγ-secreting cells but is dispensable for host protection against Mycobacterium tuberculosis infection.PloS one · 2013Article
- Within the Enemy's Camp: contribution of the granuloma to the dissemination, persistence and transmission of Mycobacterium tuberculosis.Frontiers in immunology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The immunological basis of tuberculin-induced necrosis, known for more than a century as "Koch's phenomenon," remains poorly understood. Aerosol infection in mice with the highly virulent Mycobacterium avium strain TMC724 causes progressive pulmonary pathology strongly resembling caseating necrosis in human patients with tuberculosis. To identify the cellular and molecular mediators causing this pathology, we infected C57BL/6 mice and mice selectively deficient in recombinase activating gene (RAG)-1, alphabeta T cell receptor (TCR), gammadelta TCR, CD4, CD8, beta2-microglobulin, interferon (IFN)-gamma, interleukin (IL)-10, IL-12p35, IL-12p35/p40, or iNOS with M. avium by aerosol and compared bacterial multiplication, histopathology, and respiratory physiology in these mice. The bacterial load in the lung was similarly high in all mouse groups. Pulmonary compliance, as a surrogate marker for granulomatous infiltrations in the lung, deteriorated to a similar extent in all groups of mice, except in alphabeta TCR-knockout (KO) and IL-12-KO mice in which compliance was higher, and in IFN-gamma and inducible nitric oxide synthase-KO mice in which compliance was reduced faster. Progressive caseation of pulmonary granulomas never occurred in alphabeta TCR-KO, IL-12-KO, and IFN-gamma-KO mice and was reduced in CD4-KO mice. In summary, alphabeta TCR(+) cells and IFN-gamma are essential for the development of mycobacteria-induced pulmonary caseous necrosis. In contrast, high mycobacterial load and extensive granulomatous infiltration per se are not sufficient to cause caseation, nor is granuloma necrosis linked to the induction of nitric oxide.
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