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Critical Reviews™ in Immunology
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ISSN Imprimir: 1040-8401
ISSN En Línea: 2162-6472

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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v28.i3.40
pages 229-248

Endothelial Injury, Alarmins, and Allog raft Rejection

Deepak A. Rao
Department of Immunobiology, Section of Human and Translational Immunology, Yale University School of Medicine, New Haven, CT 06520-8089
Jordan S. Pober
Department of Immunobiology, Section of Human and Translational Immunology, Yale University School of Medicine, New Haven, CT 06520-8089

SINOPSIS

Allograft blood vessels are important targets of clinical allograft rejection. Perioperative allograft injury to graft vasculature, especially the endothelial ñåll (EC) lining, increases the risk of subsequent acute and chronic vascular rejection. We hypothesize that allograft EC injured by ischemia-reperfusion (I/R) during transplantation releases mediators, termed “alarmins,” that alter and intensify the host antigraft adaptive immune response. We begin with a review of both perioperative I/R injury to graft endothelium and T-cell-mediated vascular rejection. We then describe several alarmins that may be released from injured allografts, including interleukin (IL)-1α, ATP, monosodium urate (MSU), and high mobility group protein B1 (HMGB1). These mediators have in common the ability to induce production of IL-1 β from mononuclear phagocytes, and both isoforms of IL-1 act on T cells to enhance destructive adaptive immune responses. Therefore, we propose that IL-1 is the key alarmin that communicates graft injury to the host's adaptive immune system, and we suggest that perioperative targeting of IL-1 represents a promising strategy to attenuate the strength of rejection reactions.


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