Exogenous cathepsin G upregulates cell surface MHC class I molecules on immune and glioblastoma cells

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dc.contributor.authorGiese, Madleen
dc.contributor.authorTuriello, Nadine
dc.contributor.authorMolenda, Nicole
dc.contributor.authorPalesch, David
dc.contributor.authorMeid, Annika
dc.contributor.authorSchroeder, Roman
dc.contributor.authorBasilico, Paola
dc.contributor.authorBenarafa, Charaf
dc.contributor.authorHalatsch, Marc-Eric
dc.contributor.authorZimecki, Michal
dc.contributor.authorWesthoff, Mike-Andrew
dc.contributor.authorRainer Wirtz, Christian
dc.contributor.authorBurster, Timo
dc.date.accessioned2018-08-20T04:43:41Z
dc.date.available2018-08-20T04:43:41Z
dc.date.issued2016-10-28
dc.description.abstractMajor histocompatibility complex (MHC) class I molecules present antigenic peptides to cytotoxic T cells. During an adaptive immune response, MHC molecules are regulated by several mechanisms including lipopolysaccharide (LPS) and interferon gamma (IFN-g). However, it is unclear whether the serine protease cathepsin G (CatG), which is generally secreted by neutrophils at the site of inflammation, might regulate MHC I molecules. We identified CatG, and to a higher extend CatG and lactoferrin (LF), as an exogenous regulator of cell surface MHC I expression of immune cells and glioblastoma stem cells. In addition, levels of MHC I molecules are reduced on dendritic cells from CatG deficient mice compared to their wild type counterparts. Furthermore, cell surface CatG on immune cells, including T cells, B cells, and NK cells triggers MHC I on THP-1 monocytes suggesting a novel mechanism for CatG to facilitate intercellular communication between infiltrating cells and the respective target cell. Subsequently, our findings highlight the pivotal role of CatG as a checkpoint protease which might force target cells to display their intracellular MHC I:antigen repertoireen_US
dc.identifier.citationMadleen Giese, Nadine Turiello, Nicole Molenda, David Palesch, Annika Meid, Roman Schroeder, Paola Basilico, Charaf Benarafa, Marc-Eric Halatsch, Michal Zimecki, Mike-Andrew Westhoff, Christian Rainer Wirtz and Timo Burste. 2016. Exogenous cathepsin G upregulates cell surface MHC class I molecules on immune and glioblastoma cells. Oncotarget.en_US
dc.identifier.urihttp://nur.nu.edu.kz/handle/123456789/3387
dc.language.isoenen_US
dc.publisherOncotargeten_US
dc.rightsAttribution-NonCommercial-ShareAlike 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/us/*
dc.subjectcathepsin Gen_US
dc.subjectMHC class Ien_US
dc.subjectglioblastoma stem cellsen_US
dc.subjectlactoferrinen_US
dc.subjectCatG deficient miceen_US
dc.subjectImmunology and Microbiology Sectionen_US
dc.subjectImmune responseen_US
dc.subjectImmunityen_US
dc.titleExogenous cathepsin G upregulates cell surface MHC class I molecules on immune and glioblastoma cellsen_US
dc.typeArticleen_US
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