Class I and Class II antigens play major and distinct regulatory roles in cell interactions. The inappropriate or aberrant expression of HLA Class II antigens is a recently described feature of organ-specific autoimmune disease which has already been studied in some detail in thyroid autoimmune disease and in type I diabetes. In vitro studies have shown that IFN-γ can induce Class II expression, either alone, as in thyroid follicular cells, or in combination with other mediators like tumour necrosis factor (TNF) or lymphotoxin (LT), as in islets cells, pointing to possible mechanisms operating in vivo. Endocrine cells inappropriately expressing Class II molecules could present their own autoantigens to T(H) cells and drive the autoimmune response against the gland. Possible triggering factors may be of a non-specific nature or a latent viral infection of the endocrine cells. Alternatively, inappropriate Class II expression could be a consequence of the autoimmune response facilitating the action of the effector mechanisms of the immune system. Morphological studies in thyroid glands do not help to understand the sequence of events leading to autoimmunity but studies recently carried out in the pancreases of type I diabetics suggest that inappropriate Class II expression precedes the rest of the autoimmune phenomena. Only progress in our understanding of the role of HLA antigens in immunoregulation will make it possible to interprete properly the meaning of 'inappropriate' Class II expression.
|Journal||Bailliere's Clinical Immunology and Allergy|
|Publication status||Published - 1 Jan 1987|