Journal
ONCOTARGET
Volume 7, Issue 46, Pages 74602-74611Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.12980
Keywords
cathepsin G; MHC class I; glioblastoma stem cells; lactoferrin; CatG deficient mice; Immunology and Microbiology Section; Immune response; Immunity
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Funding
- Alexander von Humboldt Polish Honorary Research Scholarship [DPK-422-1658/2013]
- Swiss National Science Foundation [149790]
- Novartis Foundation
- EU/FP7 Marie Curie-International Reintegration Grant
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Major 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 repertoire.
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