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Title:
Pathways for antigen cross presentation | Seminars in Immunopathology
Description:
Dendritic cells (DCs) have the unique ability to capture cellular tissue antigens, and to present them on MHC class I molecules to antigen-specific CD8+ T lymphocytes after migration to the draining lymph nodes. This process, called “cross presentation” can lead either to the tolerization or activation of antigen-specific CD8+ T cells. Antigen capture is believed to occur by phagocytosis of antigen-bearing dead cells. Recent studies suggest that the antigen transferred from the phagocytosed cell to the DC during cross presentation is a proteasome substrate, rather than a proteasomal degradation product. In most cases, the formation of the peptide-MHC class I complexes in DCs requires the export of protein antigens from phagosomes to the cytosol, where they undergo proteasomal degradation. The resulting peptides are then translocated by TAP to the lumen of a cross presentation-loading compartment, for association to MHC class I under the control of chaperones and oxido-reductases. This loading compartment may be either the endoplasmic reticulum (ER) or a mix phagosome-ER compartment. MHC class I egress from the loading compartment to cell surface remains to be analyzed.
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Keywords {🔍}
google, scholar, cells, dendritic, class, cell, immunol, antigens, antigen, mhc, presentation, crosspresentation, med, exp, nature, article, protein, molecules, immunity, exogenous, usa, science, cross, endoplasmic, crosspriming, proc, natl, acad, sci, proteins, vivo, eur, biol, membrane, processing, cellular, proteasome, compartment, cytotoxic, rev, complex, maturation, content, springer, reticulum, nat, major, histocompatibility, irestricted, apoptotic,
Topics {✒️}
h-2dd pre-mrnas results class i-restricted cross-presentation month download article/chapter pa28alpha/beta proteasome regulator bone marrow-derived cells major histocompatibility complex mfg-e8-deficient mice aaa atpase cdc48/p97 antigen-bearing dead cells expand tumor-reactive cd8 epstein-barr virus-transformed bacteria-induced neo-biosynthesis dendritic cell-derived exosomes rapidly cross-present antigen dendritic cell cross-presentation retrograde protein translocation fcgamma receptor-mediated induction bevan mj vaccinia virus-derived antigens major histocompatibility antigens vaccinia virus-specific cd8 immune complex internalization article springer seminars er-phagosome fusion defines cross presentation-loading compartment tumor-derived exosomes mix phagosome-er compartment bacterial fusion protein presenting cells immature dendritic cells t-cell responses privacy choices/manage cookies dendritic cell responses cytotoxic t-cell immunity human dendritic cells antigen cross-presentation antigen cross presentation phagocytic antigen processing early antigen presentation sebastian amigorena h-2 congenic cells antigen-specific cd8+ cloned dendritic cells mouse dendritic cells developing dendritic cells dendritic cells form peptide-mhc class cytomegalovirus proteins us2 retro-translocation full article pdf
Questions {❓}
- Zinkernagel RM (2002) On cross-priming of MHC class I-specific CTL: rule or exception?
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headline:Pathways for antigen cross presentation
description:Dendritic cells (DCs) have the unique ability to capture cellular tissue antigens, and to present them on MHC class I molecules to antigen-specific CD8+ T lymphocytes after migration to the draining lymph nodes. This process, called “cross presentation” can lead either to the tolerization or activation of antigen-specific CD8+ T cells. Antigen capture is believed to occur by phagocytosis of antigen-bearing dead cells. Recent studies suggest that the antigen transferred from the phagocytosed cell to the DC during cross presentation is a proteasome substrate, rather than a proteasomal degradation product. In most cases, the formation of the peptide-MHC class I complexes in DCs requires the export of protein antigens from phagosomes to the cytosol, where they undergo proteasomal degradation. The resulting peptides are then translocated by TAP to the lumen of a cross presentation-loading compartment, for association to MHC class I under the control of chaperones and oxido-reductases. This loading compartment may be either the endoplasmic reticulum (ER) or a mix phagosome-ER compartment. MHC class I egress from the loading compartment to cell surface remains to be analyzed.
datePublished:2004-12-03T00:00:00Z
dateModified:2004-12-03T00:00:00Z
pageStart:257
pageEnd:271
sameAs:https://doi.org/10.1007/s00281-004-0176-0
keywords:
Dendritic cells
Cross presentation
MHC class I
Phagosomes
Proteasome
Immunology
Internal Medicine
Pathology
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headline:Pathways for antigen cross presentation
description:Dendritic cells (DCs) have the unique ability to capture cellular tissue antigens, and to present them on MHC class I molecules to antigen-specific CD8+ T lymphocytes after migration to the draining lymph nodes. This process, called “cross presentation” can lead either to the tolerization or activation of antigen-specific CD8+ T cells. Antigen capture is believed to occur by phagocytosis of antigen-bearing dead cells. Recent studies suggest that the antigen transferred from the phagocytosed cell to the DC during cross presentation is a proteasome substrate, rather than a proteasomal degradation product. In most cases, the formation of the peptide-MHC class I complexes in DCs requires the export of protein antigens from phagosomes to the cytosol, where they undergo proteasomal degradation. The resulting peptides are then translocated by TAP to the lumen of a cross presentation-loading compartment, for association to MHC class I under the control of chaperones and oxido-reductases. This loading compartment may be either the endoplasmic reticulum (ER) or a mix phagosome-ER compartment. MHC class I egress from the loading compartment to cell surface remains to be analyzed.
datePublished:2004-12-03T00:00:00Z
dateModified:2004-12-03T00:00:00Z
pageStart:257
pageEnd:271
sameAs:https://doi.org/10.1007/s00281-004-0176-0
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Dendritic cells
Cross presentation
MHC class I
Phagosomes
Proteasome
Immunology
Internal Medicine
Pathology
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