Experimental Mouse Models Have Been Developed to Study the Mechanisms $\beta$

Experimental mouse models have been developed to study the mechanisms leading to the breakdown of self-tolerance and the onset of autoimmunity. One strategy is to express a foreign antigen, such as a viral protein, in a single defined cell type in a peripheral organ. For instance, the lymphocytic choriomeningitis virus (LCMV) glycoprotein has been expressed in β-islet cells of the pancreas by making a line of mice that is transgenic for a construct linking the LCMV-glycoprotein gene to the insulin promoter. In these transgenic mice, the LCMV protein is expressed only in pancreatic $\beta$ -islet cells. Thymocytes with T-cell receptors specific for a peptide of LCMV-glycoprotein bound to MHC class I develop normally in the thymus, and do not undergo negative selection. The fate of these T cells once they emigrate from the thymus would likely be:

A) They would be activated in the periphery and attach and kill the pancreatic $\beta$ -islet cells.
B) They would either be deleted in the periphery or would become unresponsive.
C) They would induce an inflammatory response in the pancreas that would up-regulate co-stimulatory molecules on antigen-presenting cells.
D) They would secrete cytokines that promote T cell proliferation.
E) They would differentiate into virus-specific memory T cells that would protect mice upon infection with LCMV.