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The mechanisms by which T cells contribute to the hepatic inflammation during antigenindependent ischemia/reperfusion (I/R) are not fully understood. We analyzed the recruitment of T cells in the postischemic hepatic microcirculation in vivo and tested the hypothesis that T cells interact with platelets and activate sinusoidal endothelial cells, resulting in microvascular dysfunction followed by tissue injury. Using intravital videofluorescence microscopy, we show in mice that warm hepatic I/R ( L iver injury induced by ischemia/reperfusion (I/R) is the critical factor in delayed or lost graft function after transplantation. The hepatic microcirculation is considered as the primary target of I/R injury of the liver. [1][2][3][4] The microvascular hepatic I/R injury is initiated by the release and action of proinflammatory cytokines and oxygen radicals, which trigger upregulation of adhesion molecules, intravascular deposition of fibrinogen, and interaction of neutrophils as well as platelets with the endothelial lining of the hepatic microvasculature. [5][6][7][8] The failure of nutritive sinusoidal perfusion results in prolongation of focal hypoxia or anoxia and loss of endothelial integrity, which together lead to edema formation and oncotic necrosis. 1 Recent studies suggest that, in addition to neutrophils and platelets, T cells are involved in the induction of I/R injury of the liver. 9-11 Based on classic models of tissue injury, T cells were not suspected to play a role in postischemic tissue damage. However, the surprising protective effect of immunosuppressive drugs on the antigenindependent postischemic liver injury, 12,13 as well as reduction of hepatic postischemic damage in athymic mice, 9 point to a potential role of T cells. The mechanisms by which T cells contribute to hepatic I/R injury are

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