ArticlePloS one2014
Mycobacterium tuberculosis subverts the TLR-2-MyD88 pathway to facilitate its translocation into the cytosol.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
- Polymorphisms in Toll-Like Receptor 10 and Tuberculosis Susceptibility: Evidence from Three Independent Series.Frontiers in immunology · 2018Trial
- From pathogenesis to antigens: the key to shaping the future of TB vaccines.Frontiers in immunology · 2024Review
- TRAF6 triggers Mycobacterium-infected host autophagy through Rab7 ubiquitination.Cell death discovery · 2023Article
- Review
- TLRs in Mycobacterial Pathogenesis: Black and White or Shades of Gray.Current microbiology · 2021Review
- Host-directed therapy to combat mycobacterial infections.Immunological reviews · 2021Review
- TGFβ restricts expansion, survival, and function of T cells within the tuberculous granuloma.Cell host & microbe · 2021Article
- Ultra-low Dose Aerosol Infection of Mice with Mycobacterium tuberculosis More Closely Models Human Tuberculosis.Cell host & microbe · 2021Article
- Idiosyncratic Biogenesis of Intracellular Pathogens-Containing Vacuoles.Frontiers in cellular and infection microbiology · 2021Review
- Article
- Vitamin D modulates human macrophage response to Mycobacterium tuberculosis DNA.Tuberculosis (Edinburgh, Scotland) · 2019Article
- An autophagy-inducing and TLR-2 activating BCG vaccine induces a robust protection against tuberculosis in mice.NPJ vaccines · 2019Article
- Examining the Complex Relationship Between Tuberculosis and Other Infectious Diseases in Children.Frontiers in pediatrics · 2019Review
- Functional aspects, phenotypic heterogeneity, and tissue immune response of macrophages in infectious diseases.Infection and drug resistance · 2019Article
- Article
- The R753Q polymorphism in Toll-like receptor 2 (TLR2) attenuates innate immune responses to mycobacteria and impairs MyD88 adapter recruitment to TLR2.The Journal of biological chemistry · 2017Article
- MyD88 in Mycobacterium tuberculosis infection.Medical microbiology and immunology · 2017Review
- Overexpression of Adenylyl Cyclase Encoded by theFrontiers in cellular and infection microbiology · 2017Article
- Mcl-1 signals pathway inhibitors in mouse peritoneal macrophage apoptosis infected with the Xinjiang strain ofInternational journal of clinical and experimental pathology · 2017Article
- The regulatory role of Mcl-1 in apoptosis of mouse peritoneal macrophage infected withInternational journal of clinical and experimental pathology · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Mycobacterium tuberculosis (M.tb) has evolved mechanisms to evade its destruction in phagolysosomes, where it successfully survives and replicates within phagocytes. Recent studies have shown that virulent strains of M.tb can translocate from the phagosome into the cytosol of dendritic cells (DC). The molecular mechanisms by which virulent M.tb strains can escape the phagosome remain unknown. Here we show that the virulent M.tb strain H37Rv, but not the vaccine strain Bacille Calmette-Guérin (BCG), escapes from the phagolysosome and enters the cytosol by interfering with the TLR-2-MyD88 signaling pathway. Using H37Rv mutants, we further demonstrate that the region of difference-1 (RD-1) locus and ESAT-6, a gene within the RD-1 locus, play an important role in the capacity of M.tb to migrate from the phagosome to the cytosol of macrophages. H37Rv, BCG, H37RvΔRD1, and H37RvΔESAT6 were able to translocate to the cytosol in macrophages derived from TLR-2- and MyD88-deficient animals, whereas only virulent H37Rv was able to enter the cytosol in macrophages from wild type mice. Therefore, signaling through the TLR-2-MyD88 pathway in macrophages plays an important role in confining M.tb within phagolysomes. Virulent strains of M.tb have evolved mechanisms to subvert this pathway, thus facilitating their translocation to the cytosol and to escape the toxic microenvironment of the phagosome or phagolysosome.
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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.