Abstract
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.
Highlights
Graves’ disease (GD) and Hashimoto thyroiditis (HT) are classified as autoimmune thyroid disorders (AITD) characterized by the breakdown of self-tolerance to thyroid antigens resulting in circulation of antibodies and lymphocyte infiltration [1]
This review will focus on the role of the T regulatory (Treg) and T helper (Th) lymphocytes, and of B lymphocytes in AITD pathogenesis
AITD arise from a breakdown of self-tolerance to thyroid antigens and this process might be induced by excessive exposure to thyroid antigens, a modified self-antigen, exposure to environmental antigens that mimic a self-antigen, polyclonal immune activation, or idiotypecross-reaction of self-antigens [40]
Summary
Graves’ disease (GD) and Hashimoto thyroiditis (HT) are classified as autoimmune thyroid disorders (AITD) characterized by the breakdown of self-tolerance to thyroid antigens resulting in circulation of antibodies and lymphocyte infiltration [1]. Helper (CD4+) T cells can be subdivided into at least three main functional subtypes according to releasing cytokines, the Th1 subset (mainly involved in cell–mediated tissue-damaging reaction), the Th2 subset (driving B cells to produce antibodies in the humoral immune response), and Th17 cells (playing a role in immune responses to infectious agents and maintenance of autoimmune diseases) [31, 32].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
