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Genetic dissection of T cell receptor V beta gene requirements for spontaneous murine diabetes.

Authors
  • Shizuru, J A
  • Taylor-Edwards, C
  • Livingstone, A
  • Fathman, C G
Type
Published Article
Journal
The Journal of experimental medicine
Publication Date
Sep 01, 1991
Volume
174
Issue
3
Pages
633–638
Identifiers
PMID: 1831491
Source
Medline
License
Unknown

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.

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