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• W2056636632 startingPage "633" @default.
• W2056636632 abstract "It has been demonstrated, in certain autoimmune disease models, that pathogenic T cells express antigen receptors of limited diversity. It has been suggested that the T cells responsible for the pathogenesis of type I diabetes mellitus might similarly demonstrate restricted T cell receptor (TCR) usage. Recently, attempts have been made to identify the V beta subset(s) that initiates and/or perpetuates the antiislet response in a mouse model of spontaneous autoimmune diabetes (non-obese diabetic [NOD] mice). In studies reported here, we have bred NOD mice to a mouse strain that congenitally lacks approximately one-half of the conventional TCR V beta alleles. Included in this deletion are TCR V beta gene products previously implicated as being involved in the pathogenesis of NOD disease. By studying second backcross-intercross animals, we were able to demonstrate that this deletion of TCR V beta gene segments did not prevent the development of insulitis or diabetes." @default.
• W2056636632 created "2016-06-24" @default.
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• W2056636632 date "1991-09-01" @default.
• W2056636632 modified "2023-10-03" @default.
• W2056636632 title "Genetic dissection of T cell receptor V beta gene requirements for spontaneous murine diabetes." @default.
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• W2056636632 doi "https://doi.org/10.1084/jem.174.3.633" @default.
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