The pore-forming apolipoprotein APOL7C drives phagosomal rupture and antigen cross-presentation by dendritic cells.

Autor: Gonzales GA; Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada.; Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada., Huang S; Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada.; Department of Microbiology, Immunology, and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada., Wilkinson L; Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada.; Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada., Nguyen JA; Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada., Sikdar S; Department of Microbiology, Immunology, and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.; Alberta Children's Research Institute, Calgary, Alberta, Canada.; Arnie Charbonneau Cancer Research Institute, Calgary, Alberta, Canada., Piot C; Immunobiology Laboratory, Francis Crick Institute, London, UK., Naumenko V; Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada.; Arnie Charbonneau Cancer Research Institute, Calgary, Alberta, Canada.; Riddell Centre for Cancer Immunotherapy, Calgary, Alberta, Canada., Rajwani J; Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada.; Alberta Children's Research Institute, Calgary, Alberta, Canada.; Arnie Charbonneau Cancer Research Institute, Calgary, Alberta, Canada., Wood CM; Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada., Dinh I; Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada., Moore M; Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada.; Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada., Cedeño E; Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada.; Department of Microbiology, Immunology, and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada., McKenna N; Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada., Polyak MJ; Department of Microbiology, Immunology, and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.; Calvin, Joan and Phoebe Snyder Institute for Chronic Disease, Calgary, Alberta, Canada., Amidian S; Cell Imaging Core, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada., Ebacher V; Hotchkiss Brain Institute, Calgary, Alberta, Canada., Rosin NL; Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada., Carneiro MB; Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada.; Department of Microbiology, Immunology, and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.; Calvin, Joan and Phoebe Snyder Institute for Chronic Disease, Calgary, Alberta, Canada., Surewaard B; Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada.; Calvin, Joan and Phoebe Snyder Institute for Chronic Disease, Calgary, Alberta, Canada., Peters NC; Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada.; Department of Microbiology, Immunology, and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.; Calvin, Joan and Phoebe Snyder Institute for Chronic Disease, Calgary, Alberta, Canada., Mody CH; Department of Microbiology, Immunology, and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.; Calvin, Joan and Phoebe Snyder Institute for Chronic Disease, Calgary, Alberta, Canada., Biernaskie J; Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada., Yates RM; Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada.; Calvin, Joan and Phoebe Snyder Institute for Chronic Disease, Calgary, Alberta, Canada., Mahoney DJ; Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada.; Alberta Children's Research Institute, Calgary, Alberta, Canada.; Arnie Charbonneau Cancer Research Institute, Calgary, Alberta, Canada.; Riddell Centre for Cancer Immunotherapy, Calgary, Alberta, Canada., Canton J; Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada.; Department of Microbiology, Immunology, and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.; Riddell Centre for Cancer Immunotherapy, Calgary, Alberta, Canada.; Calvin, Joan and Phoebe Snyder Institute for Chronic Disease, Calgary, Alberta, Canada.; Hotchkiss Brain Institute, Calgary, Alberta, Canada.
Jazyk: angličtina
Zdroj: Science immunology [Sci Immunol] 2024 Nov; Vol. 9 (101), pp. eadn2168. Date of Electronic Publication: 2024 Nov 01.
DOI: 10.1126/sciimmunol.adn2168
Abstrakt: Conventional dendritic cells (cDCs) generate protective cytotoxic T lymphocyte (CTL) responses against extracellular pathogens and tumors. This is achieved through a process known as cross-presentation (XP), and, despite its biological importance, the mechanism(s) driving XP remains unclear. Here, we show that a cDC-specific pore-forming protein called apolipoprotein L 7C (APOL7C) is up-regulated in response to innate immune stimuli and is recruited to phagosomes. Association of APOL7C with phagosomes led to phagosomal rupture and escape of engulfed antigens to the cytosol, where they could be processed via the endogenous MHC class I antigen processing pathway. Accordingly, mice deficient in APOL7C did not efficiently prime CD8 + T cells in response to immunization with bead-bound and cell-associated antigens. Together, our data indicate the presence of dedicated apolipoproteins that mediate the delivery of phagocytosed proteins to the cytosol of activated cDCs to facilitate XP.
Databáze: MEDLINE
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