Complete prevention of diabetes in transgenic NOD mice expressing I-E molecules

• Published in: Immunology letters Vol. 31; no. 1; pp. 47 - 52
• Main Authors: Uno, Masashi, Miyazaki, Toru, Uehira, Masahiro, Nishimoto, Hirofumi, Kimoto, Masao, Miyazaki, Junichi, Yamamura, Ken-ichi
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 1992; Elsevier
• Subjects: Animals; Animals, Genetically Modified; Biological and medical sciences; Diabetes Mellitus, Type 1 - prevention & control; Experimental and animal immunopathology. Animal models; Gene Expression; Genetic Therapy; Histocompatibility Antigens Class II - genetics; Immunopathology; Insulitis; Islets of Langerhans - pathology; Lymphocytes - physiology; Medical sciences; MHC class II; Mice; Mice, Mutant Strains; Monocytes - physiology; Transgenic mouse; Insulitis; NOD-E α d; MMC; NOD; TdR; Transgenic mouse; GL-Phe; MHC; MHC class II; mAb; IFN; B6-E α d; MLR; PBL; Endocrinopathy; Immunopathology; Animal model; Mixed lymphocyte reaction; Pathogenesis; Major histocompatibility system; Rodentia; Class II histocompatibility antigen; Transgenic animal; Gene expression; H-2-System; Characterization; Resistance; Vertebrata; Mammalia; Mouse; Insulin dependent diabetes

Previously, we showed that transgenic expression of the MHC (major histocompatibility complex) class II I-E molecules prevented insulitis in non-obese diabetic (NOD) mice at the age of 19 weeks. To rule out the possibility that the I-E expression merely delays the onset of insulitis, we have further...