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For Research Use Only. Not For Clinical Use.


Background

Type 1 diabetes (T1D) in both humans and nonobese diabetic (NOD) mice is a chronic autoimmune disease that results from destruction of pancreatic β cells by CD4+ and CD8+ T cells targeting many antigens. A large fraction of the islet-associated CD8+ cells in NOD mice recognize the mimotopes NRP-A7 and -V7 in the context of the MHC molecule Kd. These T cells are diabetogenic, target a peptide from islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP 206-214, similar to NRP-A7 and -V7), and circulate in the blood, particularly as clinical disease nears. Another important feature of the diabetogenic CD8+ response is that it involves recognition, by smaller T cell pools, of many other IGRP epitopes and epitopes in other, even ubiquitous, autoantigens, such as dystrophia myotonica kinase (DMK). The polyspecificity of this T cell response is compounded by the fact that individual specificities harbor clones engaging pMHC over a range of avidities, the strength of which correlates with pathogenic potential.
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