Literature DB >> 3287175

Diabetes in transgenic mice resulting from over-expression of class I histocompatibility molecules in pancreatic beta cells.

J Allison1, I L Campbell, G Morahan, T E Mandel, L C Harrison, J F Miller.   

Abstract

A class I histocompatibility gene, H-2Kb, linked to the rat insulin promoter, is overexpressed in the pancreatic beta cells of transgenic mice. The mice, whether syngeneic or allogeneic to the transgene, develop insulin dependent diabetes without detectable T cell infiltration, suggesting a direct, non-immune role for the transgenic class I molecules in the disease process.

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Year:  1988        PMID： 3287175     DOI： 10.1038/333529a0

Source DB:  PubMed          Journal:  Nature        ISSN： 0028-0836            Impact factor:   49.962


  59 in total

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3.  Expression of adenoviral E3 transgenes in beta cells prevents autoimmune diabetes.

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Review 6.  Non-obese diabetic transgenic mouse.

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Journal:  Springer Semin Immunopathol       Date:  1992

7.  Low incidence of autoimmune type I diabetes in BB rats fed a hydrolysed casein-based diet associated with early inhibition of non-macrophage-dependent hyperexpression of MHC class I molecules on beta cells.

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8.  Developmental failure of chimeric embryos expressing high levels of H-2Dd transplantation antigens.

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9.  Peripheral tolerance to allogeneic class II histocompatibility antigens expressed in transgenic mice: evidence against a clonal-deletion mechanism.

Authors:  K M Murphy; C T Weaver; M Elish; P M Allen; D Y Loh
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10.  Islet inflammation and hyperplasia induced by the pancreatic islet-specific overexpression of interleukin-6 in transgenic mice.

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