Location of Repository

Escape from the Phagosome: The Explanation for MHC-I Processing of Mycobacterial Antigens?

By Melanie J. Harriff, Georgiana E. Purdy and David M. Lewinsohn

Abstract

Mycobacterium tuberculosis (Mtb) is thought to live in an altered phagosomal environment. In this setting, the mechanisms by which mycobacterial antigens access the major histocompatibility class I (MHC-I) processing machinery remain incompletely understood. There is evidence that Mtb antigens can be processed in both endocytic and cytosolic environments, with different mechanisms being proposed for how Mtb antigens can access the cytosol. Recently, electron microscopy was used to demonstrate that Mtb has the potential to escape the phagosome and reside in the cytosol. This was postulated as the primary mechanism by which Mtb antigens enter the MHC-I processing and presentation pathway. In this commentary, we will review data on the escape of Mtb from the cytosol and whether this escape is required for antigen presentation to CD8+ T cells

Topics: Immunology
Publisher: Frontiers Research Foundation
OAI identifier: oai:pubmedcentral.nih.gov:3342008
Provided by: PubMed Central
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • http://www.pubmedcentral.nih.g... (external link)
  • Suggested articles

    Preview

    Citations

    1. (1995). A phagosome-tocytosol pathway for exogenous antigens presented on MHC class I molecules.
    2. (2007). A reduced antigen load in vivo, rather than weak inflammation, causes a substantial delay in CD8+ T cell priming against Mycobacterium bovis (bacillus Calmette-Guerin).
    3. (2011). accepted: 17
    4. (1964). An electronmicroscopic study of experimental infections with acid-fast bacilli.
    5. andBloom,B.R.(1999).Mycobacterialinfectionof macrophagesresults in membrane-permeable phagosomes.
    6. andRussell,D.G.(2000).Trafficking and release of mycobacterial lipids from infected macrophages.
    7. (2009). Antigen load governs the differential priming of CD8 T cells in response to the bacille Calmette Guerin vaccine orMycobacteriumtuberculosis infection.
    8. (2003). Apoptosis facilitates antigen presentation to T lymphocytes through MHC-I and CD1 in tuberculosis.
    9. (1997). Arrest of mycobacterial phagosome maturation is caused by a block in vesicle fusion between stages controlled by rab5 and rab7.
    10. (2008). Bacterial protein secretion is required for priming of CD8+ T cells specific for the Mycobacterium tuberculosis antigen CFP10.
    11. (2004). Cell biology of mycobacterium tuberculosis phagosome.
    12. (1965). Changes in the fine structure of macrophages in experimentally produced tuberculous granulomas in hamsters.
    13. (1998). Characterization of human CD8+ T cells reactive with Mycobacterium tuberculosis-infected antigen-presentingcells.J.Exp.Med.
    14. (1995). Characterization of the Mycobacterium tuberculosis phagosome and evidence that phagosomal maturation is inhibited.
    15. (1990). Class I-restricted processing and presentation of exogenous cellassociated antigen in vivo.
    16. (1996). Comparable growth of virulent and avirulent Mycobacterium tuberculosis inhuman macrophages in vitro.
    17. Consensus statement: global burden of tuberculosis: estimated incidence, prevalence. and mortality by country. WHO Global Surveillance and Monitoring Project.
    18. (2010). Cross-presentation of peptides from intracellular pathogens by MHC class I molecules.
    19. (1976). Cross-priming for a secondary cytotoxic resonse to minor H antigens with H-2 congenic cells which do not cross-react in the cytotoxic assay.
    20. (2001). Dendritic cells: specialized and regulated antigen processing machines.
    21. (1984). Disruption of phagosomal membranes of normal alveolar macrophages by the H37Rv strain of Mycobacterium tuberculosis. A correlate of virulence.
    22. (2003). Early phagosomes in dendritic cells form a cellular compartment sufficient for cross presentation of exogenous antigens.Proc.Natl.Acad.Sci.U.S.A.
    23. (1982). Electron microscopic demonstration of close contact between intracellular mycobacteria and the phagosomal membrane.
    24. (2008). Endocytosis mechanisms and the cell biology of antigen presentation.
    25. (2002). Endoplasmic reticulummediated phagocytosis is a mechanismofentryintomacrophages.Cell 110,
    26. (2004). Enhanced protection against tuberculosis by vaccination with recombinant Mycobacterium microti vaccine that induces T cell immunity against region of difference 1 antigens.
    27. (2001). Entry and survival of pathogenic mycobacteria in macrophages.
    28. (2003). ERphagosome fusion defines an MHC class I cross-presentation compartment in dendritic cells.
    29. (2012). Escape from the phagosome: the explanation for MHC-I processing of mycobacterial antigens?
    30. (2009). Evolution of foamy macrophages in the pulmonary granulomas of experimental tuberculosis models.
    31. (2008). Foamy macrophages from tuberculous patients’ granulomas constitute a nutrient-rich reservoir for M. tuberculosis persistence.
    32. (2009). Host ER-parasitophorous vacuole interaction provides a route of entry for antigen cross-presentation in Toxoplasma gondii-infected dendritic cells.
    33. (2010). How do mycobacteriaactivateCD8+Tcells? Trends Microbiol.
    34. (2003). HumanCD8+Tcellsrecognizeepitopes of the 28-kDa hemolysin and the 38-kDa antigen of Mycobacterium tuberculosis.
    35. (2000). Identification of mycobacterial surface proteins released into subcellular compartments of infected macrophages.
    36. (2004). Important role of cathepsinSingeneratingpeptides for TAP-independent MHC class I crosspresentation in vivo.
    37. (2005). In vivo depletion of CD11c+ c e l l sd e l a y st h e CD4+ T cell response to Mycobacterium tuberculosis and exacerbates the outcome of infection.
    38. (2005). Increased vaccine efficacy against tuberculosis of recombinant Mycobacterium bovis bacille Calmette-Guerin mutants that secrete listeriolysin.
    39. (2007). Induction of CD8 T cells against a novel epitope in TB10.4: correlation with mycobacterial virulence and the presence of a functional region of difference-1.
    40. (2005). Influence of ESAT-6 secretion system 1 (RD1) of Mycobacterium tuberculosis on the interaction between mycobacteria and the host immune system.
    41. (2010). Intracellular mechanisms of antigen cross presentation in dendritic cells.
    42. (1994). Intracellular trafficking in Mycobacterium tuberculosis and Mycobacterium aviuminfected macrophages.
    43. (2005). Ipr1 gene mediates innate immunity to tuberculosis.
    44. leprae translocate from the phagolysosome to the cytosol in myeloid cells. Cell 129, 1287–1298. VanEndert,P.(2011).Post-proteasomal and proteasome-independent generation of MHC class I ligands.
    45. (2001). Lipoprotein access to MHC class I presentation during infection of murine macrophages with live mycobacteria.
    46. (2006). Macrophage apoptosis in response to high intracellular burden of Mycobacterium tuberculosis is mediated by a novelcaspase-independentpathway.
    47. Major histocompatibility class I presentation of soluble antigen facilitated by Mycobacterium tuberculosis infection.
    48. (2012). MHC-I processing of mycobacterial antigens
    49. (2008). Mycobacterial manipulation of vacuolar sorting.
    50. (1997). Mycobacterial phagosome maturation, rab proteins, and intracellular trafficking.
    51. (2001). Mycobacterial surface moieties are released from infected macrophages by a constitutive exocytic event.
    52. (2002). Mycobacterium and the coat of many lipids.
    53. (2006). Mycobacterium avium subsp. paratuberculosis PtpA is an endogenous tyrosine phosphatase secreted during infection.
    54. (2009). Mycobacterium requires an allaround closely apposing phagosome membrane to maintain the maturation block and this apposition is re-established when it rescues itself from phagolysosomes.
    55. (2011). Mycobacterium tuberculosis induces an atypical cell death mode to escape from infected macrophages.
    56. (2007). Mycobacterium tuberculosis infects dendritic cells with high frequency and impairs their function in vivo.
    57. (1999). Mycobacterium tuberculosis phagosome.
    58. (2008). Mycobacterium tuberculosis prevents inflammasome activation.
    59. (2011). Mycobacterium tuberculosis protein tyrosine phosphatase (PtpA) excludes hostvacuolar-H+-ATPasetoinhibit phagosome acidification.
    60. (2004). Mycobacterium tuberculosis resides in nonacidified vacuoles in endocytically competent alveolar macrophages from patients with tuberculosis and HIV infection.
    61. (2008). Mycobacterium tuberculosis virulence is mediated by PtpA dephosphorylation of human vacuolar protein sorting 33B.
    62. (2001). Mycobacterium tuberculosis: here today, and here tomorrow.
    63. (1996). Mycobacterium-containing phagosomes are accessible to early endosomes and reflect a transitional state in normal phagosome biogenesis.
    64. (2003). Mycobacterium’s arrest of phagosome maturation in macrophages requires Rab5 activity and accessibility to iron.
    65. (2011). NOD2 controls the nature of the inflammatory response and subsequent fate of Mycobacterium tuberculosis and M. bovis BCG in human macrophages.
    66. (1993). Pathogenesis of tuberculosis: interaction of Mycobacterium tuberculosis with macrophages.
    67. (1993). Phagocytic processing of bacterial antigens for class I MHC presentation to T cells.
    68. (1984). Phagosomal membranes of Mycobacterium bovis BCG-immunealveolarmacrophages are resistant to disruption by Mycobacterium tuberculosis H37Rv.
    69. (2003). Phagosomes are competent organelles for antigen crosspresentation.
    70. (2006). Priming of T cells by exogenous antigen cross-presented on MHC class I molecules.
    71. (2001). Processing of exogenous antigens for presentation by class I MHC molecules involves post-Golgi peptideexchangeinfluencedbypeptideMHC complex stability and acidic pH.
    72. (2007). rabGTPase function by intracellular bacterial pathogens.
    73. (2003). Recombinant BCG exporting ESAT6 confers enhanced protection against tuberculosis.
    74. (2000). Relative contributions of distinct MHC class I-dependent cell populations in protection to tuberculosis infection in mice.
    75. (1971). Response of cultured macrophages to Mycobacterium tuberculosis, with observations on fusion of lysosomes with phagosomes.
    76. (2005). Role of CD8+ T lymphoc y t e si nc o n t r o lo fMycobacterium tuberculosis infection.
    77. (1996). Roles of proteasomes, transporter for antigen presentation (TAP), and beta2-microglobulinintheprocessing of bacterial or particulate antigens via an alternate class I MHC processingpathway.J.Immunol.156,
    78. Sec22b regulates phagosomal maturation and antigen crosspresentation by dendritic cells.
    79. (2010). Secreted immunodominant Mycobacterium tuberculosis antigens are processed by the cytosolic pathway.
    80. (2006). Secreted proteinsfromMycobacteriumtuberculosis gain access to the cytosolic MHC class-I antigen-processing pathway.
    81. (1997). Sequestration of Mycobacterium tuberculosis in tight vacuoles in vivo in lung macrophages of mice infected by the respiratory route.
    82. Tampe,R.,andKurts,C.(2008).Spatial and mechanistic separation of cross-presentation and endogenous antigen presentation.
    83. (2008). The cell biology of cross-presentation and the role of dendritic cell subsets.
    84. (2002). The Mycobacterium tuberculosis phagosome in human macrophages is isolated from the host cell cytoplasm.
    85. (1996). The Mycobacterium tuberculosis phagosome interacts with early endosomes and is accessible to exogenously administered transferrin.
    86. (2009). The Mycobacterium tuberculosis phagosome is a HLA-I processing competent organelle.
    87. (2003). The primary mechanism of attenuation of bacillus Calmette-Guerin is a loss of secreted lytic function required for invasion of lung interstitial tissue.
    88. This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits noncommercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.
    89. (1927). Tubercule bacilli in latent tuberculous lesions and in lung tissue withouttuberculouslesions.Arch.Pathol.
    90. (2007). Type VII secretion – mycobacteria show the way.
    91. (2006). Virulent clinical isolates of Mycobacterium tuberculosis grow rapidly and induce cellular necrosis but minimal apoptosis in murinemacrophages.J.Leukoc.Biol.
    92. (2000). Virulent Mycobacterium tuberculosis strains evade apoptosis of infected alveolar macrophages.

    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.