ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Mycobacterium tuberculosis and TLR2 agonists inhibit induction of type I IFN and class I MHC antigen cross processing by TLR9.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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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
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Delayed-Type Hypersensitivity toInternational journal of molecular sciences · 2026Pooled it
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- Novel prophylactic and therapeutic multi-epitope vaccine based on Ag85A, Ag85B, ESAT-6, and CFP-10 of Mycobacterium tuberculosis using an immunoinformatics approach.Osong public health and research perspectives · 2024Article
- Protein Expression of TLR2, TLR4, and TLR9 on Monocytes in TB, HIV, and TB/HIV.Journal of immunology research · 2024Article
- Mutations in genes encoding innate immune molecules identified in bladder cancer samples as potential biomarkers for immunotherapy with BCG and agonists.Frontiers in urology · 2023Article
- In-depth systems biological evaluation of bovine alveolar macrophages suggests novel insights into molecular mechanisms underlyingFrontiers in microbiology · 2022Article
- MyD88-dependent BCG immunotherapy reduces tumor and regulates tumor microenvironment in bladder cancer murine model.Scientific reports · 2021Article
- NFκB-Activated COX2/PGECancers · 2021Article
- A Role of Intracellular Toll-Like Receptors (3, 7, and 9) in Response toInternational journal of molecular sciences · 2020Review
- March ofClinical & translational immunology · 2020Review
- FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Vitamin D modulates human macrophage response to Mycobacterium tuberculosis DNA.Tuberculosis (Edinburgh, Scotland) · 2019Article
- Association of Toll like receptor 2 and 9 gene variants with pulmonary tuberculosis: exploration in a northern Indian population.Molecular biology reports · 2018Article
- Impaired IFN-α-mediated signal in dendritic cells differentiates active from latent tuberculosis.PloS one · 2018Article
- Protein O-mannosylation deficiency increases LprG-associated lipoarabinomannan release by Mycobacterium tuberculosis and enhances the TLR2-associated inflammatory response.Scientific reports · 2017Article
- Badger macrophages fail to produce nitric oxide, a key anti-mycobacterial effector molecule.Scientific reports · 2017Article
- Cellular Decision Making by Non-Integrative Processing of TLR Inputs.Cell reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Dendritic cells (DCs) cross process exogenous Ags and present them by class I MHC (MHC-I) molecules to CD8(+) T cells specific for Ags from viruses and bacteria such as Mycobacterium tuberculosis. Unmethylated CpG DNA signals through TLR9 to induce type I IFN (IFN-alpha/beta), which enhances MHC-I Ag cross processing, but lipoproteins that signal through TLR2 do not induce IFN-alpha/beta. In these studies we observed that M. tuberculosis, which expresses agonists of both TLR9 and TLR2, did not induce production of IFN-alpha/beta or cross processing by murine DCs. Furthermore, M. tuberculosis and TLR2 agonists inhibited induction of IFN-alpha/beta and DC cross processing by CpG DNA. Exogenous IFN-alpha/beta effectively enhanced cross processing of M. bovis bacillus Calmette-Guérin expressing OVA, bypassing the inhibition of induction of endogenous IFN-alpha/beta. In addition, inhibition of TLR9-induced cross processing of M. bovis bacillus Calmette-Guérin expressing OVA could be circumvented by pretreating cells with CpG DNA to induce IFN-alpha/beta and MHC-I cross processing before inhibitory mycobacterial TLR2 agonists were present. Inhibition of the response to one TLR by another may affect the ultimate response to pathogens like M. tuberculosis that express agonists of multiple TLRs, including TLR2 and TLR9. This mechanism may contribute to immune evasion and explain why IFN-alpha/beta provides little contribution to host immunity to M. tuberculosis. However, downregulation of certain TLR responses may benefit the host by preventing detrimental excessive inflammation that may occur in the presence of persistent infection.
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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.