ArticleCell host & microbe2016
Antigen Export Reduces Antigen Presentation and Limits T Cell Control of M. tuberculosis.
Article in Cell host & microbe, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 110 citations in OpenAlex.
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- Impaired IFNγ responsiveness of monocyte-derived lung cells limits immunity to Mycobacterium tuberculosis.Nature communications · 2026Article
- HowVaccines · 2026Review
- Enhanced tuberculosis control via leveraging dendritic cell-mediated Th1 responses in preventive and immunotherapeutic vaccine strategies.Journal of advanced research · 2026Article
- A CD40-OX40 co-stimulatory circuit orchestrates protective CD4Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
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- Downregulated Plasma-Derived Extracellular Vesicle MicroRNAs as Novel Biomarkers for Enhanced Tuberculosis Diagnosis.Journal of immunology research · 2026Article
- Multi-epitope design against emerging nipah virus towards peptide vaccine development.Bioinformation · 2026Article
- T cell-macrophage interactions in tuberculosis: What we've got here is failure to communicate.Journal of internal medicine · 2026Review
- Impaired IFNγ responsiveness of monocyte-derived lung cells limits immunity tobioRxiv : the preprint server for biology · 2025Article
- Finding and filling the knowledge gaps in mechanisms of T cell-mediated TB immunity to inform vaccine design.Nature reviews. Immunology · 2025Review
- Macrophage-T cell interactions promote SLAMF1 expression for enhanced TB defense.Nature communications · 2025Article
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- MAIT cells protect against sterile lung injury.Cell reports · 2025Article
- Iron-restricted Mycobacterium tuberculosis exports pathogenicity factors packed in extracellular vesicles.PloS one · 2025Article
- Investigation of the relationship between chronic hepatitis B and tuberculosis using bioinformatics and systems biology approaches.Frontiers in medicine · 2025Article
- Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Persistence of Mycobacterium tuberculosis results from bacterial strategies that manipulate host adaptive immune responses. Infected dendritic cells (DCs) transport M. tuberculosis to local lymph nodes but activate CD4 T cells poorly, suggesting bacterial manipulation of antigen presentation. However, M. tuberculosis antigens are also exported from infected DCs and taken up and presented by uninfected DCs, possibly overcoming this blockade of antigen presentation by infected cells. Here we show that the first stage of this antigen transfer, antigen export, benefits M. tuberculosis by diverting bacterial proteins from the antigen presentation pathway. Kinesin-2 is required for antigen export and depletion of this microtubule-based motor increases activation of antigen-specific CD4 T cells by infected cells and improves control of intracellular infection. Thus, although antigen transfer enables presentation by bystander cells, it does not compensate for reduced antigen presentation by infected cells and represents a bacterial strategy for CD4 T cell evasion.
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