Immunopathological findings and thyroid autoantibodies in thyroid autonomy

Different phenomena under consideration, lymphocytic and macrophagic infiltration and increased thyrocyte class I and class II antigen expression, normally ascribed to autoimmune thyroid disease (Graves' disease; Hashimoto's thyroiditis) were frequently found in thyroid glands with autonomous nodules, too. Contrary, nodular formations in the vast majority of nodular goiters were not associated with these immunopathological findings. Furthermore, thyroid microsomal, anti-peroxidase and TSH-receptor antibodies although at low frequency rates, were only detected in cases of autonomous nodules but not in cases of nodular goiters. From these findings we conclude that the immune phenomenon observed in thyroid autonomy could not be a consequence of nodular formations but that at least in some cases of thyroid autonomy immunopathogenic mechanisms may play an important role. Based on the fact that class I hyper-expression was more common and that a stronger correlation of cell infiltration with increased class I than with increased class II expression on thyrocytes existed we propose, that if the initial event of the autoimmune process is indeed increased class II expression, this stimulus may more likely originate from increased non-thyrocyte class II positivity (for example dendritic or endothelial cells) than from thyrocyte class II positivity. But, if aberrant class II expression is not the initial stimulus, another candidate could be the increased thyrocyte class I expression observed, probably due to the action of interferon alpha and/or beta induced by any unknown stimulus (viruses?).