Hyperexpression of GAD in the islets may be relevant but is it sufficient to induce autoimmune insulitis?

In their article, Drs. Degli Esposti and Mackay propose a mechanism whereby an islet antigen glutamic acid decarboxylase (GAD) could be hyperexpressed on islet cells, resulting in an aggressive immune attack on that cell with consequent destruction, loss of insulin secretory capacity and thus insulin-dependent diabetes mellitus (IDDM). It is our purpose to present briefly the many different mechanisms whereby self or non-self antigens might become targets of the immune response and progress to IDDM. Since the precise nature of the target antigen, if it exists, is unresolved, we think that the interesting mechanism proposed by Degli Esposti and Mackay, whereby stress