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

摘要: Major histocompatibility complex (MHC) class I molecules present antigenic peptides to cytotoxic T cells. During an adaptive immune response, MHC 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 generally secreted neutrophils at site of inflammation, might regulate molecules. We identified CatG, a higher extend CatG lactoferrin (LF), as exogenous regulator cell surface expression cells glioblastoma stem In addition, levels reduced on dendritic from deficient mice compared their wild type counterparts. Furthermore, cells, B NK triggers THP-1 monocytes suggesting novel mechanism for facilitate intercellular communication between infiltrating respective target cell. Subsequently, our findings highlight pivotal role checkpoint force display intracellular I:antigen repertoire.