ArticleInfection and immunity2008
Bacterial protein secretion is required for priming of CD8+ T cells specific for the Mycobacterium tuberculosis antigen CFP10.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Control of antigen presentation on MHC-I by a bacterial secretion system.bioRxiv : 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
- Design and Characterization of a Multistage Peptide-Based Vaccine Platform to TargetBioconjugate chemistry · 2023Article
- High Bacillary Burden and the ESX-1 Type VII Secretion System Promote MHC Class I Presentation by Mycobacterium tuberculosis-Infected Macrophages to CD8 T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Immunopeptidomics reveals determinants ofeLife · 2023Article
- Article
- Mycobacterium tuberculosis-specific CD4+ and CD8+ T cells differ in their capacity to recognize infected macrophages.PLoS pathogens · 2018Article
- Cross-priming induces immunodomination in the presence of viral MHC class I inhibition.PLoS pathogens · 2018Article
- Mycobacterial Hsp65 antigen upregulates the cellular immune response of healthy individuals compared with tuberculosis patients.Human vaccines & immunotherapeutics · 2017Article
- Identification of Mycobacterial RplJ/L10 and RpsA/S1 Proteins as Novel Targets for CD4Infection and immunity · 2017Article
- Human and Murine Clonal CD8+ T Cell Expansions Arise during Tuberculosis Because of TCR Selection.PLoS pathogens · 2015Article
- Orchestration of pulmonary T cell immunity during Mycobacterium tuberculosis infection: immunity interruptus.Seminars in immunology · 2014Review
- Mycobacterium tuberculosis-specific CD8+ T cells are functionally and phenotypically different between latent infection and active disease.European journal of immunology · 2013Article
- Article
- Antigen-specific CD8(+) T cells and protective immunity to tuberculosis.Advances in experimental medicine and biology · 2013Review
- Escape from the Phagosome: The Explanation for MHC-I Processing of Mycobacterial Antigens?Frontiers in immunology · 2012Article
- Regulation of neutrophils by interferon-γ limits lung inflammation during tuberculosis infection.The Journal of experimental medicine · 2011Article
- Bacteria modulate the CD8+ T cell epitope repertoire of host cytosol-exposed proteins to manipulate the host immune response.PLoS computational biology · 2011Article
- Lipids, apoptosis, and cross-presentation: links in the chain of host defense against Mycobacterium tuberculosis.Microbes and infection · 2011Review
- T cell monitoring of chemotherapy in experimental rat tuberculosis.Antimicrobial agents and chemotherapy · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Mycobacterium tuberculosis infection elicits antigen-specific CD8(+) T cells that are required to control disease. It is unknown how the major histocompatibility complex class I (MHC-I) pathway samples mycobacterial antigens. CFP10 and ESAT6 are important virulence factors secreted by M. tuberculosis, and they are immunodominant targets of the human and murine T-cell response. Here, we test the hypothesis that CFP10 secretion by M. tuberculosis is required for the priming of CD8(+) T cells in vivo. Our results reveal an explicit dependence upon the bacterial secretion of the CFP10 antigen for the induction of antigen-specific CD8(+) T cells in vivo. By using well-defined M. tuberculosis mutants and carefully controlling for virulence, we show that ESX-1 function is required for the priming of CD8(+) T cells specific for CFP10. CD4(+) and CD8(+) T-cell responses to mycobacterial antigens secreted independently of ESX-1 were unaffected, suggesting that ESX-1-dependent phagosomal escape is not required for CD8(+) T-cell priming during infection. We propose that the overrepresentation of secreted proteins as dominant targets of the CD8(+) T-cell response during M. tuberculosis infection is a consequence of their preferential sampling by the MHC-I pathway. The implications of these findings should be considered in all models of antigen presentation during M. tuberculosis infection and in vaccine development.
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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.