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(Circulation. 2006;114:1561-1564.)
© 2006 American Heart Association, Inc.

Editorial

Th1 Adaptive Immune Responses in Cardiac Graft Arteriosclerosis

Deleterious or Beneficial?

George Tellides, MD, PhD

From the Interdepartmental Program in Vascular Biology and Transplantation and the Department of Surgery, Yale University School of Medicine, New Haven, Conn.

Correspondence to George Tellides, MD, PhD, 295 Congress Ave, BCMM 454, New Haven, CT 06510. E-mail george.tellides@yale.edu

Key Words: Editorials • arteriosclerosis • infection • inflammation • transplantation

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Heart transplants are not rejected in the absence of adaptive immune responses, eg, in transplantations between genetically identical donors and hosts or to recipients with severe combined immunodeficiencies. Activation of adaptive immunity to an allograft causes destructive responses against donor parenchymal or vascular cells, called acute rejection. In the presence of adequate immunosuppression, acute rejection is suppressed; however, chronic rejection may occur, manifesting as conduit arterial lumen loss resulting from expansion of the tunica intima and remodeling of vessel size, called graft arteriosclerosis.¹ The differences in pathological findings and in sensitivity to immunosuppressive agents suggest that chronic graft failure arises from different mechanisms operative in separate allograft compartments than in acute graft rejection. The precise pathogenesis of graft arteriosclerosis is unknown, although there is broad consensus that it is, at least in part, an alloimmune process in that the arteriosclerotic changes are limited to the vascular bed of the allograft and spare the host vasculature. Adaptive immunity may activate a variety of effector mechanisms that cause chronic graft rejection in murine transplantation models.¹ Although it is not the only factor that can cause graft arteriosclerosis, the evidence for the signature Th1 cytokine, interferon (IFN)-, is particularly compelling. In mouse transplantation models, serological neutralization or the genetic absence of IFN- reduces intimal expansion of graft arteries.^2,3 Moreover, in a chimeric human-mouse model, antibody neutralization of IFN- prevents allogeneic T cell–mediated endothelial dysfunction, intimal thickening, and outward vascular remodeling; administration of IFN- accelerates these effects; and exogenous IFN- in the absence . . . [Full Text of this Article]

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