Assignment task:
Some early studies aimed at deciphering the mechanisms involved in breakdown of tolerance in autoimmune disease, were based on generating transgenic mice that constitutively expressed a viral protein in the beta-islet cells of the pancreas. These mice were crossed to transgenic mice expressing a T-cell receptor specific for MHC class I bound to a peptide of this viral protein. The double transgenic mice generated large numbers of CD8 T cells capable of recognizing this viral antigen on beta-islet cells, yet the mice never spontaneously developed type I diabetes, a disease in which beta-islet cells are destroyed by T cells. This lack of response most likely reflects:
A. The deletion of all the antigen-specific T cells by central tolerance mechanisms in the thymus
B. The fact that beta-islet cells in the pancreas are femuinnnumber, and therefore unable to generate enough antigen to prime T cell responses
C. The absence of CD4 T cells that recognize the same viral antigen
D. The absence of infection or tissue damage needed to trigger the priming of viral protein-specific T cells