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Diabetes 52:1111-1118, 2003
© 2003 by the American Diabetes Association, Inc.

A New Murine Model of Islet Xenograft Rejection

Graft Destruction Is Dependent on a Major Histocompatibility–Specific Interaction Between T-Cells and Macrophages

Peter Schmidt1, Henrik Krook1, Akira Maeda2, Olle Korsgren1, and Birgitta Benda1

1 Division of Clinical Immunology, Uppsala University, Uppsala, Sweden
2 Department of Transplantation Surgery, Karolinska Hospital, Huddinge, Sweden

A new murine model of porcine islet-like cell cluster (ICC) xenograft rejection, avoiding interference of unspecific inflammation, was introduced and used to investigate rejection mechanisms. Athymic (nu/nu) mice were transplanted with syngeneic, allogeneic, or xenogeneic islets under the kidney capsule. After the original transplantation, immune cells in porcine ICC xenografts undergoing rejection in native immunocompetent mice were transferred to the peritoneal cavity of the athymic mice. At defined time points after transfer, the primary grafts were evaluated by immunohistochemistry and real-time quantitative RT-PCR to estimate cytokine and chemokine mRNA expression. Transfer of immunocompetent cells enabled athymic (nu/nu) mice to reject a previously tolerated ICC xenograft only when donor and recipient were matched for major histocompatibility complex (MHC). In contrast, allogeneic and syngeneic islets were not rejected. The ICC xenograft rejection was mediated by transferred T-cells. The main effector cells, macrophages, were shown to be part of a specific immune response. By day 4 after transplantation, there was an upreglation of both Th1- and Th2-associated cytokine transcripts. The transferred T-cells were xenospecific and required MHC compatibility to induce rejection. Interaction between the TCR of transferred T-cells and MHC on host endothelial cells and/or macrophages seems necessary for inducing ICC xenograft rejection.


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Copyright © 2003 by the American Diabetes Association.