Xenoreactive natural antibodies (XNA) and complement (C) are thought to be the two major inciting factors that result in hyperacute rejection (HAR) of an immediately vascularized, discordant xenograft within minutes to a very few hours, with destruction and infarction of the transplanted organ. If recipients are modified by various experimental modalities, such as removal and suppression of XNA-and C-mediated responses, thus avoiding HAR, the process of delayed xenograft rejection (DXR) with a significant vascular component still occurs after a delay of several days or, at the most, a few weeks (Bach et al. 1993). The end result in both instances is the invariable and unacceptable loss of xenografts, which currently limits application of xenotransplantation beyond experimental protocols.

The mechanisms underlying DXR are far from clear but appear not necessarily to involve XNA-and C-mediated responses as those noted in HAR. Moreover, DXR can occur without the prominent participation of T lymphocytes. One of us (FHB) has suggested that the final common pathogenic mechanisms underly-