ArticleImmunology2002
Immunological basis of the development of necrotic lesions following Mycobacterium avium infection.
Article in Immunology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 51 citations in OpenAlex.
- Progression and Dissemination of Pulmonary Mycobacterium Avium Infection in a Susceptible Immunocompetent Mouse Model.International journal of molecular sciences · 2022Article
- Prospective study of immunomodulation in osteoarticular tuberculosis non responsive to anti tubercular therapy.Journal of clinical orthopaedics and trauma · 2018Article
- Review
- The tuberculosis necrotizing toxin kills macrophages by hydrolyzing NAD.Nature structural & molecular biology · 2015Article
- 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
- The Warburg effect in mycobacterial granulomas is dependent on the recruitment and activation of macrophages by interferon-γ.Immunology · 2015Article
- Two state model for a constant disease hazard in paratuberculosis (and other bovine diseases).Veterinary research · 2015Article
- Chemokines in tuberculosis: the good, the bad and the ugly.Seminars in immunology · 2014Review
- Dynamics of immune effector mechanisms during infection with Mycobacterium avium in C57BL/6 mice.Immunology · 2013Article
- Nitric oxide inhibits the accumulation of CD4+CD44hiTbet+CD69lo T cells in mycobacterial infection.European journal of immunology · 2012Article
- Immunotherapy against the radial glia marker GLAST effectively triggers specific antitumor effectors without autoimmunity.Oncoimmunology · 2012Article
- Article
- The death-promoting molecule tumour necrosis factor-related apoptosis inducing ligand (TRAIL) is not required for the development of peripheral lymphopenia or granuloma necrosis during infection with virulent Mycobacterium avium.Clinical and experimental immunology · 2011Article
- Mycobacterium tuberculosis culture filtrate proteins plus CpG Oligodeoxynucleotides confer protection to Mycobacterium bovis BCG-primed mice by inhibiting interleukin-4 secretion.Infection and immunity · 2009Article
- Mycobacteria-induced granuloma necrosis depends on IRF-1.Journal of cellular and molecular medicine · 2009Article
- A role for tumour necrosis factor-alpha, complement C5 and interleukin-6 in the initiation and development of the mycobacterial cord factor trehalose 6,6'-dimycolate induced granulomatous response.Microbiology (Reading, England) · 2008Article
- Regulation of granuloma fibrosis by nitric oxide during Mycobacterium avium experimental infection.International journal of experimental pathology · 2006Article
- Article
- Pathogenesis of Mycobacterium avium infection: typical responses to an atypical mycobacterium?Immunologic research · 2006Review
- Gamma interferon-induced T-cell loss in virulent Mycobacterium avium infection.Infection and immunity · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Normal C57BL/6 mice infected with 106 colony-forming units of a highly virulent strain of Mycobacterium avium developed a progressive infection characterized by loss of T cells from the tissues and infiltration with high numbers of heavily infected macrophages. In contrast, when C57BL/6 mice were infected with 102 colony-forming units of the same strain they retained T cells and T-cell reactivity in the tissues, and granulomas evolved into large masses that, at 4 months of infection, exhibited central necrosis. The development of these necrotic lesions did not occur in nude mice, nor in mice genetically deficient in CD4, interleukin-12 (IL-12) p40, interferon-gamma (IFN-gamma) and CD40 and were reduced in mice deficient in CD54 or IL-6. They were less numerous but bigger in mice deficient in IL-10 or the inducible nitric oxide synthase, correlating with the increased resistance to mycobacterial proliferation of these strains as compared to control mice. The appearance of necrosis was not affected in mice deficient in CD8alpha, T-cell receptor delta, tumour necrosis factor receptor p55, and perforin, nor was it affected in mice over-expressing bcl2. The appearance of necrosis could be prevented by administering antibodies specific for CD4, IL-12p40, or IFN-gamma from the second month of infection when organized granulomas were already found. Our results show that the immunological mediators involved in the induction of protective immunity are also major players in the immunopathology associated with mycobacteriosis.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.