ArticleThe Journal of experimental medicine2001
Processing of Mycobacterium tuberculosis antigen 85B involves intraphagosomal formation of peptide-major histocompatibility complex II complexes and is inhibited by live bacilli that decrease phagosome maturation.
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 53 papers.
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Who cites it
53 citing papers in PubMed, 124 citations in OpenAlex.
- Trial
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- Sorting nexin 5 mediates antigen presentation and immunity againstbioRxiv : the preprint server for biology · 2026Article
- Finding and filling the knowledge gaps in mechanisms of T cell-mediated TB immunity to inform vaccine design.Nature reviews. Immunology · 2025Review
- Prevention of tuberculosis in cynomolgus macaques by an attenuated Mycobacterium tuberculosis vaccine candidate.Nature communications · 2025Article
- TheFrontiers in immunology · 2024Article
- Article
- Human M1 macrophages express unique innate immune response genes after mycobacterial infection to defend against tuberculosis.Communications biology · 2022Article
- A recombinant bovine adenoviral mucosal vaccine expressing mycobacterial antigen-85B generates robust protection against tuberculosis in mice.Cell reports. Medicine · 2021Article
- A guide to measuring phagosomal dynamics.The FEBS journal · 2021Review
- Genome-Wide Gene Expression Analysis of Mtb-Infected DC Highlights the Rapamycin-Driven Modulation of Regulatory CytokinesFrontiers in immunology · 2021Article
- NOD2/RIG-I ActivatingFrontiers in immunology · 2020Article
- Immunology ofMicrobiology spectrum · 2019Review
- Immunometabolic Signatures Predict Risk of Progression to Active Tuberculosis and Disease Outcome.Frontiers in immunology · 2019Article
- An autophagy-inducing and TLR-2 activating BCG vaccine induces a robust protection against tuberculosis in mice.NPJ vaccines · 2019Article
- Rapid loss of early antigen-presenting activity of lymph node dendritic cells against Ag85A protein following Mycobacterium bovis BCG infection.BMC immunology · 2018Article
- Mycobacterium tuberculosis Exploits a Molecular Off Switch of the Immune System for Intracellular Survival.Scientific reports · 2018Article
- Mycobacterium tuberculosis-induced miR-155 subverts autophagy by targeting ATG3 in human dendritic cells.PLoS pathogens · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mycobacterium tuberculosis (MTB) inhibits phagosomal maturation to promote its survival inside macrophages. Control of MTB infection requires CD4 T cell responses and major histocompatibility complex (MHC) class II (MHC-II) processing of MTB antigens (Ags). To investigate phagosomal processing of MTB Ags, phagosomes containing heat-killed (HK) or live MTB were purified from interferon-gamma (IFN-gamma)-activated macrophages by differential centrifugation and Percoll density gradient subcellular fractionation. Flow organellometry and Western blot analysis showed that MTB phagosomes acquired lysosome-associated membrane protein-1 (LAMP-1), MHC-II, and H2-DM. T hybridoma cells were used to detect MTB Ag 85B(241-256)-I-A(b) complexes in isolated phagosomes and other subcellular fractions. These complexes appeared initially (within 20 min) in phagosomes and subsequently (>20 min) on the plasma membrane, but never within late endocytic compartments. Macrophages processed HK MTB more rapidly and efficiently than live MTB; phagosomes containing live MTB expressed fewer Ag 85B(241-256)-I-A(b) complexes than phagosomes containing HK MTB. This is the first study of bacterial Ag processing to directly show that peptide-MHC-II complexes are formed within phagosomes and not after export of bacterial Ags from phagosomes to endocytic Ag processing compartments. Live MTB can alter phagosome maturation and decrease MHC-II Ag processing, providing a mechanism for MTB to evade immune surveillance and enhance its survival within the host.
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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.