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J. Exp. Med.,
Volume 187, Number 12, June 15, 1998 1985-1993
By
From the * Section of Immunobiology, the B7-1 transgene expression on the pancreatic islets in nonobese diabetic (NOD) mice leads to
accelerated diabetes, with >50% of animals developing diabetes before 12 wk of age. The expression of B7-1 directly on the pancreatic Section of Endocrinology, and the § Howard Hughes Medical
Institute, Yale University School of Medicine, New Haven, Connecticut 06510
cells, which do not normally express costimulator
molecules, converts the cells into effective antigen-presenting cells leading to an intensified autoimmune attack. The pancreatic islet infiltrate in diabetic mice consists of CD8 T cells, CD4
T cells, and B cells, similar to diabetic nontransgenic NOD mice. To elucidate the relative importance of each of the subsets of cells, the NOD-rat insulin promoter (RIP)-B7-1 animals
were crossed with NOD.2microglobulin 
/ mice which lack major histocompatibility
complex class I molecules and are deficient in peripheral CD8 T cells, NOD.CD4 / mice
which lack T cells expressing CD4, and NOD.µMT / mice which lack B220-positive B
cells. These experiments showed that both CD4 and CD8 T cells were necessary for the accelerated onset of diabetes, but that B cells, which are needed for diabetes to occur in normal
NOD mice, are not required. It is possible that B lymphocytes play an important role in the
provision of costimulation in NOD mice which is unnecessary in the NOD-RIP-B7-1 transgenic mice.
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