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Journal of Experimental Medicine, Vol 173, 1091-1097, Copyright © 1991 by Rockefeller University Press
ARTICLES |
N Nakano, H Kikutani, H Nishimoto and T Kishimoto
Institute for Molecular and Cellular Biology, Osaka University, Japan.
Five islet-reactive T cell clones were established from islet- infiltrating T cells of non-obese diabetic (NOD) mice. All clones expressed CD4, but not CD8, and responded to islet cells from various strains of mice in the context of I-ANOD. They could induce insulitis when transferred into disease-resistant I-E+ transgenic NOD mice. The T cell receptor (TCR) sequences utilized by the clones were determined. Their usage of TCR V and J segments was not restricted but was rather diverse. One of the clones utilized V beta 16. The expression of V beta 16 was significantly reduced in I-E+ transgenic NOD, suggesting the possibility that the islet-reactive T cell clone expressing V beta 16 may be deleted or inactivated by I-E molecules. This clone might be one of the candidates that triggers insulitis.
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