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Transgenic Expression of CD95 Ligand on Islet β Cells Induces a Granulocytic Infiltration but does not Confer Immune Privilege upon Islet Allografts
Janette Allison, Harry M. Georgiou, Andreas Strasser and David L. Vaux
Proceedings of the National Academy of Sciences of the United States of America
Vol. 94, No. 8 (Apr. 15, 1997), pp. 3943-3947
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/41935
Page Count: 5
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Binding of CD95 (Fas/APO-1) by its ligand (CD95L) commonly induces apoptosis. Apoptosis of activated T cells, induced by CD95L expressed in the rodent testis, has been proposed to be the mechanism of immune privilege [Bellgrau, D., Gold, D., Selawry, H., Moore, J., Franzusoff, A. & Duke, R. C. (1995) Nature (London) 377, 630-632]. To test whether CD95L could protect pancreatic islet grafts from rejection, we made transgenic mice expressing murine CD95L on their islet β cells and transplanted fetal pancreata under the kidney capsules of allogeneic animals. Expression of CD95L failed to protect the grafts from rejection. However, transgenic mice developed a granulocytic infiltration in their pancreata. These results demonstrate a pro-inflammatory function of CD95L and suggest that expression of CD95L may not be sufficient to protect organ allografts.
Proceedings of the National Academy of Sciences of the United States of America © 1997 National Academy of Sciences