Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. Immunohistochemistry reveals pancreatic islet cell expression of the transgene and no expression in the spleen, kidney or thymus. Isolated islets stain normally for insulin and are morphologically indistinguishable from control islets. Additional functional studies found no expression in bone marrow. Histology revealed no insulitis and the single transgenic mice do not become diabetic. T-cell proliferation assays, Cytotoxic Lymphocyte (CTL) assays, and adoptive transfer studies performed using transgenic mice indicate significantly reduced class 1 and class II T-cell responses compared to controls. Hemagglutination inhibition assays of sera from HA primed transgenic mice indicate antibody titers slightly lower but nearly equivalent to HA primed control mice. Antibody titers of all transgenic mice tested were significantly higher than preimmune levels. When mated with Tg(TcraCl4,TcrbCl4) mice, the double transgenic neonates become spontaneously diabetic after birth and die within 10 days. <p> This is a good model for studying peripheral tolerance.

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These mice carry a transgene on a BALB/cBy background that expresses the influenza hemagglutinin (HA) on pancreatic islet beta cells that results in reduced class 1 and class II T-cell responses in cytotoxic lymphocyte (CTL) assays and adoptive transfer studies.

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