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Article: Kinesin-1 regulates antigen cross-presentation through the scission of tubulations from early endosomes in dendritic cells

TitleKinesin-1 regulates antigen cross-presentation through the scission of tubulations from early endosomes in dendritic cells
Authors
Keywordsanimal cell
animal experiment
animal model
animal tissue
antigen degradation assay
Issue Date2020
PublisherNature Research (part of Springer Nature): Fully open access journals. The Journal's web site is located at http://www.nature.com/ncomms/index.html
Citation
Nature Communications, 2020, v. 11, p. article no. 1817 How to Cite?
AbstractDendritic cells (DCs) constitute a specialized population of immune cells that present exogenous antigen (Ag) on major histocompatibility complex (MHC) class I molecules to initiate CD8 + T cell responses against pathogens and tumours. Although cross-presentation depends critically on the trafficking of Ag-containing intracellular vesicular compartments, the molecular machinery that regulates vesicular transport is incompletely understood. Here, we demonstrate that mice lacking Kif5b (the heavy chain of kinesin-1) in their DCs exhibit a major impairment in cross-presentation and thus a poor in vivo anti-tumour response. We find that kinesin-1 critically regulates antigen cross-presentation in DCs, by controlling Ag degradation, the endosomal pH, and MHC-I recycling. Mechanistically, kinesin-1 appears to regulate early endosome maturation by allowing the scission of endosomal tubulations. Our results highlight kinesin-1’s role as a molecular checkpoint that modulates the balance between antigen degradation and cross-presentation.
Persistent Identifierhttp://hdl.handle.net/10722/290046
ISSN
2023 Impact Factor: 14.7
2023 SCImago Journal Rankings: 4.887
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBelabed, M-
dc.contributor.authorMauvais, FX-
dc.contributor.authorMaschalidi, S-
dc.contributor.authorKurowska, M-
dc.contributor.authorGoudin, N-
dc.contributor.authorHuang, JD-
dc.contributor.authorFischer, A-
dc.contributor.authorde Saint Basile, G-
dc.contributor.authorvan Endert, P-
dc.contributor.authorSepulveda, FE-
dc.contributor.authorMénasché, G-
dc.date.accessioned2020-10-22T08:21:18Z-
dc.date.available2020-10-22T08:21:18Z-
dc.date.issued2020-
dc.identifier.citationNature Communications, 2020, v. 11, p. article no. 1817-
dc.identifier.issn2041-1723-
dc.identifier.urihttp://hdl.handle.net/10722/290046-
dc.description.abstractDendritic cells (DCs) constitute a specialized population of immune cells that present exogenous antigen (Ag) on major histocompatibility complex (MHC) class I molecules to initiate CD8 + T cell responses against pathogens and tumours. Although cross-presentation depends critically on the trafficking of Ag-containing intracellular vesicular compartments, the molecular machinery that regulates vesicular transport is incompletely understood. Here, we demonstrate that mice lacking Kif5b (the heavy chain of kinesin-1) in their DCs exhibit a major impairment in cross-presentation and thus a poor in vivo anti-tumour response. We find that kinesin-1 critically regulates antigen cross-presentation in DCs, by controlling Ag degradation, the endosomal pH, and MHC-I recycling. Mechanistically, kinesin-1 appears to regulate early endosome maturation by allowing the scission of endosomal tubulations. Our results highlight kinesin-1’s role as a molecular checkpoint that modulates the balance between antigen degradation and cross-presentation.-
dc.languageeng-
dc.publisherNature Research (part of Springer Nature): Fully open access journals. The Journal's web site is located at http://www.nature.com/ncomms/index.html-
dc.relation.ispartofNature Communications-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectanimal cell-
dc.subjectanimal experiment-
dc.subjectanimal model-
dc.subjectanimal tissue-
dc.subjectantigen degradation assay-
dc.titleKinesin-1 regulates antigen cross-presentation through the scission of tubulations from early endosomes in dendritic cells-
dc.typeArticle-
dc.identifier.emailHuang, JD: jdhuang@hku.hk-
dc.identifier.authorityHuang, JD=rp00451-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/s41467-020-15692-0-
dc.identifier.pmid32286311-
dc.identifier.pmcidPMC7156633-
dc.identifier.scopuseid_2-s2.0-85083488861-
dc.identifier.hkuros316039-
dc.identifier.volume11-
dc.identifier.spagearticle no. 1817-
dc.identifier.epagearticle no. 1817-
dc.identifier.isiWOS:000528789000007-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl2041-1723-

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