Hori et al. demonstrated that cDCs acquire MHC-I complexes from dead cells in a process called cross-dressing, which requires recognition of phosphatidylserine on dying cells independent of efferocytosis. Acquisition was shown to occur via direct association of membrane fragments with DCs, and not internalization or membrane fusion. While both cross-presentation and cross-dressing induced substantial T cell proliferation in vitro, cross-dressing played a minimal role in vivo at steady state. However, addition of the inflammatory TLR3 ligand polyI:C to B2M-knockout mice injected with tumor cells greatly enhanced T cell proliferation.
Contributed by Morgan Janes
ABSTRACT: In addition to cross-presentation, cross-dressing plays an important role in the induction of CD8(+) T cell immunity. In the process of cross-dressing, conventional dendritic cells (DCs) acquire major histocompatibility complex class I (MHCI) from other cells and subsequently prime CD8(+) T cells via the pre-formed antigen-MHCI complexes without antigen processing. However, the mechanisms underlying the cross-dressing pathway, as well as the relative contributions of cross-presentation and cross-dressing to CD8(+) T cell priming are not fully understood. Here, we demonstrate that DCs rapidly acquire MHCI-containing membrane fragments from dead cells via the phosphatidylserine recognition-dependent mechanism for cross-dressing. The MHCI dressing is enhanced by a TLR3 ligand polyinosinic-polycytidylic acid (polyI:C). Further, polyI:C promotes not only cross-presentation but also cross-dressing in vivo. Taken together, these results suggest that cross-dressing as well as cross-presentation is involved in inflammatory diseases associated with cell death and type I IFN production.
Author Info: (1) Laboratory of Immunology and Microbiology, College of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Shiga 525-8577, Japan. (2) Laboratory of Immunology and Microbio
Author Info: (1) Laboratory of Immunology and Microbiology, College of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Shiga 525-8577, Japan. (2) Laboratory of Immunology and Microbiology, College of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Shiga 525-8577, Japan. (3) Laboratory of Immunology and Microbiology, College of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Shiga 525-8577, Japan. (4) Laboratory of Immunology and Microbiology, College of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Shiga 525-8577, Japan. (5) Laboratory of Immunology and Microbiology, College of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Shiga 525-8577, Japan. (6) Department of Immunology, Kanazawa University Graduate School of Medical Sciences, 13-1 Takara-machi, Kanazawa, Ishikawa 920-8640, Japan. WPI Nano Life Science Institute (NanoLSI), Kanazawa University, Kakuma-machi, Kanazawa, Ishikawa 920-1192, Japan. (7) Department of Immunology, Kanazawa University Graduate School of Medical Sciences, 13-1 Takara-machi, Kanazawa, Ishikawa 920-8640, Japan. WPI Nano Life Science Institute (NanoLSI), Kanazawa University, Kakuma-machi, Kanazawa, Ishikawa 920-1192, Japan. (8) Laboratory of Immunology and Microbiology, College of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Shiga 525-8577, Japan. Research Center for Animal Life Science, Shiga University of Medical Sciences, Seta, Tsukinowa-cho, Otsu, Shiga 520-2192, Japan.
