Grave’s Disease: Pathophysiology of a Model Autoimmune Disease

Grave's disease is categorized as an autoimmune disease and type V hypersensitivity. It causes the formation of IgG antibodies that stimulates the thyrotropin receptor. It is suggested that in this disease, there is hyper stimulation of the thyroid gland by different clinical researches of this disease that result in thyrocyte hypoplasia (which is also known as goiter) and hyperthyroidism. Vulnerability to factors impacting the defenselessness and triggers for Graves' infection endures, alongside a wide variety in the reaction to hostile thyroid medications, as of now at roughly half of the non-responders. This review article describes the immune genetic, pathophysiological as well as environmental aspects related to this disease. It also emphasizes new research that elucidates the new methods to help resolve this disease-however its various areas of concern still need to be explored more extensively. by the action of CD90 glycoprotein. Fibroblasts are accelerated into adipogenesis by some factors such as IL-16, PGD2, and, IL-1β. Research shows that adipogenesis is inhibited by the action of TNF-α and IFNγ 15. The output of these researches concludes that cytokines instead of tissue remodeling and fibrosis are involved in the early phases of ophthalmopathy. The Thy1+ fibroblasts are capable of developing into myofibroblasts. Myofibroblasts are present in muscles and participate in important functions such as collagen accumulation and muscle contractions18. The antiadipogenic factors released by Thy1+ fibroblasts inhibit the differentiation of Thy1− fibroblasts. The introduction of TGF-β and the quantity of Thy1- and Thy1+ causes extraocular muscle and the involvement of adipose tissue in GO patients19. B-cells are the type of white blood cells that originate from hematopoietic stem cells and mature in the bone marrow. B cells are activated in secondary lymphoid organs -i.e. spleen and lymph nodes. They function in humoral immunity and produce antibodies.