| Sec22b regulates phagosomal maturation and antigen crosspresentation by dendritic cells. | |
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MedLine Citation:
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PMID: 22153078 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Antigen (Ag) crosspresentation by dendritic cells (DCs) involves the presentation of internalized Ags on MHC class I molecules to initiate CD8+ T cell-mediated immunity in response to certain pathogens and tumor cells. Here, we identify the SNARE Sec22b as a specific regulator of Ag crosspresentation. Sec22b localizes to the ER-Golgi intermediate compartment (ERGIC) and pairs to the plasma membrane SNARE syntaxin 4, which is present in phagosomes (Phgs). Depletion of Sec22b inhibits the recruitment of ER-resident proteins to Phgs and to the vacuole containing the Toxoplasma gondii parasite. In Sec22b-deficient DCs, crosspresentation is compromised after Ag phagocytosis or endocytosis and after invasion by T. gondii. Sec22b silencing inhibited Ag export to the cytosol and increased phagosomal degradation by accelerating lysosomal recruitment. Our findings provide insight into an intracellular traffic pathway required for crosspresentation and show that Sec22b-dependent recruitment of ER proteins to Phgs critically influences phagosomal functions in DCs. |
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Authors:
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Ignacio Cebrian; Geraldine Visentin; Nicolas Blanchard; Mabel Jouve; Alexandre Bobard; Catarina Moita; Jost Enninga; Luis F Moita; Sebastian Amigorena; Ariel Savina |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Cell Volume: 147 ISSN: 1097-4172 ISO Abbreviation: Cell Publication Date: 2011 Dec |
Date Detail:
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Created Date: 2011-12-13 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0413066 Medline TA: Cell Country: United States |
Other Details:
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Languages: eng Pagination: 1355-68 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 Elsevier Inc. All rights reserved. |
Affiliation:
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Institut Curie, INSERM U932, Immunité et Cancer, 26 rue d'Ulm, 75248 Paris Cedex 05, France. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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