Influence of thyroid hormone in the expression of the marker pro-apoptosis BID, in spite of the predominance of anti-apoptosis activation in intratiroidal lymphocytic infiltration in Hashimoto’s thyroiditis

Cell destruction in Hashimoto's thyroiditis (HT) involves autoantibodies and cytotoxic T lymphocytes. Thyrocytes maintenance occurs by pro-apoptotic, anti-apoptotic and cell proliferation balance. To characterize factors related to the mechanisms of apoptosis and cell proliferation in thyroid cells and intrathyroid lymphocytic infiltrate in HT. We assessed lymphocytic infiltrate and thyroid cells from HT and normal thyroid by immunohistochemical analysis of cell proliferation (Ki-67), antiproliferation (p27Kip1), pro-apoptosis (Fas, Fas-ligand, BID) and anti-apoptosis (MCL-1, BCL2) markers. Lymphocytic infiltrate presented BCL2 and MCL-1 higher expression, Ki-67 and p27kip1 balance. Thyrocytes exhibited Fas and FasL balance, higher BID expression; MCL-1, BCL-2, Ki-67 similar to the normal thyroid. T4 and higher lymphocytes BID expression were associated. In lymphocytic infiltrate predominated anti-apoptosis in relation to pro-apoptosis except for BID. Thyrocytes presented pro-apoptosis and anti-apoptosis balance and cell proliferation similar to normal thyroid. T4-associated BID expression in HT lymphocytes suggests the influence of thyroid hormone as a signal to up-regulate the BID pro-apoptotic protein and thus increase lymphocytic apoptosis rates. •Thyroid lymphocytes infiltration in Hashimoto's thyroiditis presented high cell proliferation, especially in the germinal centers indicating chronic inflammatory activity.•In Hashimoto's thyroiditis thyrocytes, cell proliferation and antiproliferation were not relevant processes comparing to individuals without autoimmune disease.•T4-associated BID in intra-thyroid lymphocytes suggests that thyroid hormone would increase lymphocytes apoptosis in Hashimoto's thyroiditis.