Diabetes in transgenic mice resulting from over-expression of class I histocompatibility molecules in pancreatic beta cells.
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.
Allison
J
J
Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia.
Campbell
I L
IL
Morahan
G
G
Mandel
T E
TE
Harrison
L C
LC
Miller
J F
JF
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000235:genetics* / Q000503:physiopathology; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics* / Q000503:physiopathology; D005786:Gene Expression Regulation; D006183:H-2 Antigens / Q000235:genetics* / Q000502:physiology; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000473:pathology / Q000503:physiopathology*; D008214:Lymphocytes / Q000503:physiopathology; D051379:Mice; D008822:Mice, Transgenic / Q000502:physiology*; D011401:Promoter Regions, Genetic; D013934:Thymectomy
D006183:H-2 Antigens; D007328:Insulin