Pancreatic islet B cells express class I but not class II antigens, and removal of Ia positive passenger cells from H-2 allogeneic islets by anti-Ia serum and complement leads to permanent allograft survival. A test was made of whether the same result can be achieved by genetically removing the Ia stimulus by performing mouse islet allografts in congenic donor-recipient combinations differing at the H-2 K only, D only, or K + D regions. Mice disparate for class I antigens (H-2 K, D, and K + D) alone reject islet allografts, suggesting that Ia positive passenger cells may be involved in presentation of class I disparities. Established islet allografts appear to be sensitive to rejection induced by injection of donor strain splenocytes when donor and recipient differ for class I (H-2 D alone and D + I) but not class II (H-2 I alone) antigens. These results are consistent with the hypothesis that pancreatic islet allografts do not express class II target antigens, but do express class I antigens that in long-established pancreatic islet allografts are capable of acting as targets but not in initiating an immune response.
Bibliographical noteFunding Information:
’ Supported-in part by NIH Grants AM1308 and AI/ GM1 7687 and Grant SMF 157-82 from the Minnesota Medical Foundation, and grants from the Juvenile Diabetes Foundation, Juvenile Diabetes Association, Inc., and the Harriet Walter-Paul L. Uhich Pancreatic Islet Transplant ResearchM emorial Fund. Dr. Morrow is a recipient of NIH Research Training Grant 1F 32AM0677 1. This is publication No., 320 from the Immunobiology Research Center. ’ To whom correspondences hould be addresseda t Box 314 Mayo, University of Minnesota Hospital, 420 Delaware Street, S.E., Minneapolis, Minn. 55455.
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