title: [Sterile inflammatory response to ischemia-reperfusion injury: immediate and long term consequences on graft function].
abstract: Solid organs used for transplantation are subjected to ischemia-reperfusion, which induces cellular stress and tissue necrosis. Ischemia-reperfusion injury activates the complement cascade and triggers the release of danger-associated molecular signals. The latter bind to pattern-recognition receptors on innate immune cells, thereby eliciting a sterile inflammatory response that, together with complement activation, increases tissue damage. This sterile inflammatory response also triggers maturation of antigen-presenting cells (macrophages and dendritic cells), enabling them to present donor antigens efficiently to recipient lymphocytes. By initiating adaptive alloimmune responses in the recipient, innate immunity plays a central role in the rejection process, which remains a major cause of late graft failure. Strategies capable of dampening the sterile inflammatory response induced by ischemia-reperfusion could therefore be beneficial, both for immediate post-transplantation graft function and for long-term outcome.
authors.affiliation: Immunologie clinique et transplantation rénale, Hôpital Edouard Herriot, 5 place d'Arsonval, 69437 Lyon, et Inserm U851. olivier.thaunatpast@free.fr
authors.forename: Olivier
authors.initials: O
authors.lastname: Thaunat
mesh_terms: D056704:Adaptive Immunity; D003165:Complement System Proteins / Q000378:metabolism*; D003713:Dendritic Cells / Q000276:immunology; D006084:Graft Rejection / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D008264:Macrophages / Q000276:immunology; D016377:Organ Transplantation; D015427:Reperfusion Injury / Q000209:etiology / Q000276:immunology*
chemical_list: D003165:Complement System Proteins