About this Research Topic
Cross-priming serves to activate cytotoxic T lymphocytes for immune defense against viruses and tumors and plays an important role in vaccinations. Only certain DC subsets can cross-present and these are characterized by expression of cell surface markers like CD8a, CD24 CD103, BDCA-3 or XCR1. Classifying DC subsets by such markers is convenient for flow-cytometric analysis, but does not mechanistically explain why a cell can cross-present. Recent studies have proposed two mechanistic explanations, which are not mutually exclusive: 1. only cross-presenting DCs possess the antigen processing machinery that loads endocytosed antigen onto MHC class I molecules (e.g. by proteases like IRAP). 2. cross-presentation depends on distinct endocytosis mechanisms (Mannose receptor, DNGR1, DC-SIGN, DEC205) (CD205) that can introduce antigen directly into distinct organelle(s) in which cross-presentation occurs. This Research Topic is focused on articles that can help understanding how cross-presentation occurs mechanistically, with a special emphasis on further endocytosis receptors, intracellular organelles and molecular antigen processing or membrane translocation mechanisms that can facilitate or are associated with cross-presentation and that can be exploited for vaccine optimization.
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