THE NONESSENTIAL ROLE OF A HUMORAL ANTIBODY RESPONSE IN ACUTE RAT CARDIAC ALLOGRAFT REJECTION

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Abstract
Progressive microvascular endothelial damage is a characteristic feature of fulminant acute cardiac allograft rejection in the rat. Serial ultrastructural tracer studies using i.v. administered colloidal carbon and horseradish peroxidase were performed in an adoptive transfer model to determine the role of cellular and humoral immune mechanisms in the pathogenesis of endothelial injury in this setting. Sublethally irradiated (780 rad) Lewis recipients of Wistar-Furth cardiac allografts reconstituted with unfractionated syngeneic immune spleen cells (2 .times. 107) or with inocula depleted of SIg+ [surface Ig] cells (1 .times. 107) were studied at days 5-7 posttransplantation, and the ultrastructural tracer data were correlated with recipient alloantibody titers. The progression microcirculatory endothelial damage within rejecting cardiac allografts was similar when recipients were reconstituted with unfractionated immune spleen cells or with SIg- cells, and the serial changes present were comparable to those documented in unmodified 1st-set rejection in this strain combination. Unreconstituted controls showed no apparent microvascular alterations. A significant alloantibody response was confined to recipients reconstituted with unfractionated immune spleen cells. All unreconstituted recipients and recipients that received splenic inocula depleted of SIg+ cells (SIg-) lacked detectable antibody in the study period. A humoral antibody response is not essential for induction of endothelial damage in fulminant acute rejection of rat cardiac allografts.