Kazunori Murata

TL;DR: The rationale for the use of C4d as a marker of antibody-mediated rejection, along with the clinical evidence supporting its use, are summarized and mechanisms by which C4D can be activated by the classical and lectin pathways of complement activation are identified.

TL;DR: It is demonstrated using a skin transplant model that alloantibody indirectly induces platelet activation and rolling in vivo and that platelets recruit leukocytes to sites of alloantsibody deposition and sustain leukocyte–endothelial cell interactions in vivo.

TL;DR: A novel role for non‐complement‐activating alloantibodies and MBL in humoral rejection is suggested, as demonstrated in mice reconstituted with monoclonal antibodies to MHC class I antigens.

TL;DR: C4d deposition is not limited to the capillaries, but extends throughout the arterial tree, and despite formation of a covalent bond, C4d is cleared within days.

TL;DR: It is indicated that IgG1 Allo-mAbs to major histocompatibility complex class I antigens can augment graft injury by stimulating EC to produce MCP-1 and by activating mononuclear cells through their Fc receptors.