TRANSGENIC EXPRESSION OF CD95 LIGAND ON ISLET BETA-CELLS INDUCES A GRANULOCYTIC INFILTRATION BUT DOES NOT CONFER IMMUNE PRIVILEGE UPON ISLET ALLOGRAFTS
J. Allison et al., TRANSGENIC EXPRESSION OF CD95 LIGAND ON ISLET BETA-CELLS INDUCES A GRANULOCYTIC INFILTRATION BUT DOES NOT CONFER IMMUNE PRIVILEGE UPON ISLET ALLOGRAFTS, Proceedings of the National Academy of Sciences of the United Statesof America, 94(8), 1997, pp. 3943-3947
Binding of CD95 (Fas/APO-1) by its ligand (CD95L) commonly induces apo
ptosis. Apoptosis of activated T cells, induced by CD95L expressed in
the rodent testis, has been proposed to be the mechanism of immune pri
vilege [Bellgrau, D., Gold, D., Selawry, H., Moore, J., Franzusoff, A.
& Duke, R. C. (1995) Nature (London) 377, 630-632]. To test whether C
D95L could protect pancreatic islet grafts from rejection, we made tra
nsgenic mice expressing murine CD95L on their islet beta cells and tra
nsplanted fetal pancreata under the kidney capsules of allogeneic anim
als. Expression of CD95L failed to protect the grafts from rejection.
However, transgenic mice developed a granulocytic infiltration in thei
r pancreata. These results demonstrate a pro-inflammatory function of
CD95L and suggest that expression of CD95L may not be sufficient to pr
otect organ allografts.