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Autoimmune thyroid disorders (AITD) broadly include Graves' disease and Hashimoto's thyroiditis which are the most common causes of thyroid gland dysfunctions. These disorders develop due to complex interactions between environmental and genetic factors and are characterized by reactivity to self-thyroid antigens due to autoreactive lymphocytes escaping tolerance. Both cell-mediated and humoral responses lead to tissue injury in autoimmune thyroid disease. The differentiation of CD4+ cells in the specific setting of immune mediators (for example cytokines, chemokines) results in differentiation of various T cell subsets. T cell identification has shown a mixed pattern of cytokine production indicating that both subtypes of T helper, Th1 and Th2, responses are involved in all types of AITD. Furthermore, recent studies described T cell subtypes Th17 and Treg which also play an essential role in pathogenesis of AITD. This review will focus on the role of the T regulatory (Treg) and T helper (Th) (especially Th17) lymphocytes, and also of B lymphocytes in AITD pathogenesis. However, we have much more to learn about cellular mechanisms and interactions in AITD before we can develop complete understanding of AITD pathophysiology.
Rydzewska et al. (Tue,) studied this question.