The histopathology of skin allograft rejection has been studied at both the light and electron microscopic levels in several species including man (1–4). Most authors are agreed that rejection of “first set” grafts is characterized by perivascular accumulations of mononuclear cells which subsequently extend throughout the substance of the graft. The mechanism of graft destruction by these infiltrating cells is uncertain and may involve vessel damage with consequent stasis of blood flow and ischemia (2–4) or direct cytotoxic action on graft parenchymal cells (2, 5). Because of the characteristic histology, and for other reasons, graft rejection has been considered an example of delayed hypersensitivity (5), although it is recognized that circulating antibody may destroy grafts in certain instances (3). We have recently investigated several lesions which have been generally regarded as delayed hypersensitivity, using refined light and electron microscopic methods (6–8).