Crosstalk between the tumor microenvironment and immune response in thyroid cancer
Autoimmune thyroid disease is caused by thyroid autoantibodies and may present with hypothyroidism, euthyroid, or hyperthyroidism (1). Thyroid antibodies include antibodies to thyroglobulin (Tg), thyroid peroxidase (TPO), thyroid stimulating hormone receptor (TSHR), sodium/iodide symporter (NIS), pendrin, and thyroid hormones (2). Hashimoto’s thyroiditis (HT) and Graves’ disease (GD) are the two major types of autoimmune thyroid disease and share lymphocytic infiltration of the thyroid parenchyma and alteration of thyroid morphology and function (2). Many retrospective studies on surgical specimens over the last decade have shown a strong positive association between papillary thyroid cancer (PTC) risk and HT (3,4). Paradoxically, patients with PTC coexisting with HT had favorable clinical outcomes compared to those without HT (4). However, the role of GD in thyroid cancer development, growth and progression is still debated.