Some Early Studies Aimed at Deciphering the Mechanisms Involved in Immunological

Multiple Choice

Some early studies aimed at deciphering the mechanisms involved in immunological tolerance, and its breakdown in cases of 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 few in number, 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 fact that the pancreas is an immune privileged site
E) The absence of infection or tissue damage needed to trigger the priming of effector T cell responses