The cause(s) of autoimmune Addisons disease is(are) still unknown. Expression of MHC class 11 antigens, suggested as a key event in the initiation and/or maintenance of organ-specific autoimmunity, occurs in normal adrenals and, therefore, is unlikely to be the primary etiologic event of Addisons disease. Defects in HLA-DQ(3 chain, found in IDDM, have not been reported in patients with Addisons disease. On the other hand, a deficiency of T suppressor cell activity was noted by some authors. To date, restricted T cell receptor (TCR) usage, alterations of the idiotype-anti-idiotype network and changes in the balance of the cytokine network have not been demonstrated in autoimmune Addisons disease.

Environmental agents (e.g. microorganisms and/or xenobiotics) might cause adrenal autoimmunity by modifying autoantigens (so that they are no longer recognized as self), releasing tissue components normally absent from the circulation, or sharing antigens with tissues (molecular mimicry). In addition, they could inhibit T suppressor cells, stimulate T helper cells, B cells or macrophages, interfere with the idiotype-anti-idiotype network, alter tissue MHC expression and finally cause changes in the production of cytokines and lymphokines. However, none of these possibilities have yet been demonstrated in autoimmune Addisons disease.

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