An autoantigen being recognized by specific receptors is the key react
ion of an autoimmune disease. Whereas much efforts have been made to d
evelop immunosuppressive regimens which reduce the amount of effector
cells, and/or inhibit receptor activation, surprisingly little attenti
on has been paid to reduce the ligand-receptor interaction by interfer
ing with the amount of antigen being presented from the target cells.
In this review, we discuss clinical observations in autoimmune endocri
ne disease which illustrate that target cell alterations can modify th
e disease activity and comment on recent clinical trials which indicat
e that beta-cell rest may be beneficial to the course of human autoimm
une diabetes mellitus.