Figure 2.

Possible roles of accelerated A^g7 protein turnover in autoimmune pathogenesis in NOD mice. (A) Model adapted from (26) and (27), linking A^g7 polymorphism to intrinsic stability defects, accelerated turnover, impaired T-cell tolerance, and increased risk of autoimmunity. (B) Revised model, based on (53), showing accelerated A^g7 turnover in vivo to be regulated, independently of structural polymorphisms and SDS instability, by unknown environmental factors, with either a neutral or inhibitory role in autoimmune pathogenesis.