MHC class I signaling: new functional perspectives for an old molecule.
Donor-specific antibodies are associated with refractory rejection episodes and poor allograft outcomes in solid organ transplantation. Our understanding of antibody-mediated allograft injury is expanding beyond complement deposition. In fact, unique mechanisms of alloantibodies are advancing our knowledge about transplant vasculopathy and antibody-mediated rejection. These include direct effects on the endothelium, resulting in the recruitment of leukocytes, chemokine and cytokine production, and stimulation of innate and adaptive alloresponses. These effects will be the focus of the following review.
Mattel Children's Hospital UCLA, Division of Pediatric Nephrology, Los Angeles, CA, USA.
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D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology / Q000517:prevention & control; D049109:Cell Proliferation / Q000502:physiology; D016207:Cytokines / Q000096:biosynthesis; D004730:Endothelium, Vascular / Q000166:cytology; D006084:Graft Rejection / Q000188:drug therapy / Q000276:immunology; D015395:Histocompatibility Antigens Class I / Q000276:immunology*; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007518:Isoantibodies / Q000276:immunology*; D009131:Muscle, Smooth, Vascular / Q000166:cytology; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use; D015398:Signal Transduction / Q000276:immunology
D016207:Cytokines; D015395:Histocompatibility Antigens Class I; D007166:Immunosuppressive Agents; D007518:Isoantibodies; D047428:Protein Kinase Inhibitors
alloantibodies; antibody-mediated rejection; complement; endothelium; human leukocyte antigen class I; therapy; transplant vasculopathy