ArticleImmunology2006
Mycobacteria lacking the RD1 region do not induce necrosis in the lungs of mice lacking interferon-gamma.
Article in Immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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Who cites it
18 citing papers in PubMed, 41 citations in OpenAlex.
- The role of ESAT-6 in tuberculosis immunopathology.Frontiers in immunology · 2024Review
- EspB and HtpG interact with the type III-A CRISPR/Cas system ofFrontiers in molecular biosciences · 2023Article
- Mycobacterium marinum down-regulates miR-148a in macrophages in an EsxA-dependent manner.International immunopharmacology · 2019Article
- Editorial: Cellular and Molecular Mechanisms ofFrontiers in cellular and infection microbiology · 2019Article
- An outbreak of tuberculosis due to Mycobacterium bovis infection in a pack of English Foxhounds (2016-2017).Transboundary and emerging diseases · 2018Article
- Necrosis Driven Triglyceride Synthesis Primes Macrophages for Inflammation DuringFrontiers in immunology · 2018Article
- Lysosomal Cathepsin Release Is Required for NLRP3-Inflammasome Activation byFrontiers in immunology · 2018Article
- Role of alpha-crystallin, early-secreted antigenic target 6-kDa protein and culture filtrate protein 10 as novel diagnostic markers in osteoarticular tuberculosis.Journal of orthopaedic translation · 2016Review
- Mouse models of human TB pathology: roles in the analysis of necrosis and the development of host-directed therapies.Seminars in immunopathology · 2016Review
- Mycobacterium tuberculosis subverts the TLR-2-MyD88 pathway to facilitate its translocation into the cytosol.PloS one · 2014Article
- Immune regulatory activities of early secreted antigenic target of 6-kD protein of Mycobacterium tuberculosis and implications for tuberculosis vaccine design.Tuberculosis (Edinburgh, Scotland) · 2011Review
- Contrasting transcriptional responses of a virulent and an attenuated strain of Mycobacterium tuberculosis infecting macrophages.PloS one · 2010Article
- Acute immune response to Mycobacterium massiliense in C57BL/6 and BALB/c mice.Infection and immunity · 2010Article
- Potential role for ESAT6 in dissemination of M. tuberculosis via human lung epithelial cells.Molecular microbiology · 2010Article
- MyBASE: a database for genome polymorphism and gene function studies of Mycobacterium.BMC microbiology · 2009Article
- Evidence for pore formation in host cell membranes by ESX-1-secreted ESAT-6 and its role in Mycobacterium marinum escape from the vacuole.Infection and immunity · 2008Article
- Disseminated disease severity as a measure of virulence of Mycobacterium tuberculosis in the guinea pig model.Tuberculosis (Edinburgh, Scotland) · 2008Article
- ESAT-6 from Mycobacterium tuberculosis dissociates from its putative chaperone CFP-10 under acidic conditions and exhibits membrane-lysing activity.Journal of bacteriology · 2007Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
The genetic region of difference 1 (RD1) in Mycobacterium tuberculosis has recently been hypothesized to encode for proteins that are cytotoxic to the host cell in nature. We demonstrate here that while M. tuberculosis grew progressively in the lungs of gene disrupted mice (GKO) unable to produce interferon-gamma (IFN-gamma), similar mice infected instead with M. bovis bacillus Calmette-Guérin (BCG) reproducibly exhibited an obvious slowing of the disease after about 20 days. Closer examination of BCG-infected GKO mice showed a florid granulomatous inflammation in the lungs, whereas similar mice infected with M. tuberculosis exhibited wholesale progressive necrosis. In the BCG-infected GKO mice large numbers of activated effector T cells, some strongly positive for the cytokine tumour necrosis factor, as well as activated natural killer cells accumulated in the lungs. To further test the hypothesis that the differences observed were directly associated with the loss of the RD1 region, it was then shown that a mutant of M. tuberculosis lacking RD1 grew progressively in both normal and GKO mice but failed to induce any degree of necrosis in either animal despite reaching similar levels in the lungs. However, when mice were infected with this mutant, in which the RD1 region had been restored by complementation, wholesale necrosis of the lungs again occurred. These data support the hypothesis that proteins encoded in the RD1 region are a major cause of necrosis and contribute significantly to the pathogenesis of the disease.
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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.