[Inflammation and rejection].
The inflammation represents an important cause of allograft tissue lesions during ongoing rejection episodes. Such inflammation is mediated, at least in part, via the release of different soluble mediators. Some of these endogenous inflammation mediators are well known and include prostaglandins, leukotriens, histamine or histaminergic compounds and factors induced by the activation of the complement cascade (C3a, C5a). More recently, different molecules have been characterized, namely cytokines that are potent mediators of both immune and inflammatory reactions. Cytokines are produced by a wide variety of cells types (i.e., inducing immune and non immune cells) and expressing pleiotropic effects. The synergism between these various inflammation mediators finally provoke the anatomopathological lesions characteristic of a rejection process that are vascular lesions, edema formation and white blood cell chemotaxis leading to massive cellular infiltration. The aim of this brief review is to analyze the more recent data of the literature concerning cytokines that, applied to the field of organ transplantation, may provide further insights onto the relationships existing between inflammation and allograft rejection.
Chatenoud
L
L
INSERM U 25, CNRS UA 122, Hôpital Necker, Paris.
Bach
J F
JF
D016207:Cytokines / Q000502:physiology*; D006084:Graft Rejection; D006801:Humans; D007249:Inflammation; D007372:Interferons / Q000502:physiology; D007375:Interleukin-1 / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D016207:Cytokines; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D007372:Interferons
Inflammation et rejet.