Graves’ Disease (GD) is an autoimmune disease characterized by an enlarged and overactive thyroid gland. The main pathogenetic mechanism of GD is the stimulation of the thyroid-stimulating hormone receptor (TSH-R), by autoantibodies that act as agonists promoting thyrocyte proliferation and activity. The complex pathogenetic interplay of GD includes genetic and environmental factors. Although the exact mechanism is still elusive, new advances over the last few years have provided evidence on the role of the microbiota, as well as the polymorphisms of several elements involved in the immune checkpoint and immune response regulation, such as PTPN22, CTLA-4, CD-40, and FCRL3. Recently, new molecules such as Iscalimab and K1-70, that target various steps in the pathogenesis of GD, have been tested, with encouraging results. Furthermore, antigen-specific immunotherapy with a combination of two TSH-R peptides has been proposed. GD affects primarily the thyroid, but extrathyroidal manifestations can be observed, namely Graves’ orbitopathy (GO), pretibial mixedema, and acropachy. Among them, GO is the most common and it is considered an autoimmune syndrome affecting orbital fibroadipose tissue, due to an interplay between cellular and humoral immunity against TSH-R and possibly other autoantigens, including insulin-like growth factor receptor (IGF-1R), shared by thyroid epithelial cells and orbital fibroblasts. Recent advances in understanding GO pathogenesis have allowed the development of new-target-based therapies. The primary goal of this special issue is to discuss novel acquisition in GD and GO pathogenesis and propose novel treatment options. We invite contributions that explore thyroid autoimmune diseases, with particular interest in GD and its extrathyroidal manifestations.

Through this special issue, we aim to contribute the improvement of the available knowledge on GD and GO promoting refinement in patient management. We welcome researchers from various disciplines to provide interdisciplinary perspectives on GD and GO. Your contributions will play a crucial role in advancing knowledge in this field.

Articles welcomed: Original research articles, review articles, case reports, case series.