TRANSGENIC EXPRESSION OF CD95 LIGAND ON ISLET BETA-CELLS INDUCES A GRANULOCYTIC INFILTRATION BUT DOES NOT CONFER IMMUNE PRIVILEGE UPON ISLET ALLOGRAFTS

Citation
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
Citations number
20
Categorie Soggetti
Multidisciplinary Sciences
ISSN journal
00278424
Volume
94
Issue
8
Year of publication
1997
Pages
3943 - 3947
Database
ISI
SICI code
0027-8424(1997)94:8<3943:TEOCLO>2.0.ZU;2-1
Abstract
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.