Abstract
Thyroid-associated ophthalmoapthy (TAO) is the most common orbital disease. As an autoimmune disorder, it is caused by self-reactive lymphocytes that escape immune tolerance, but the mechanism is not fully understood. The basic process of TAO is the infiltration of immune cells in orbital tissues, the activation of orbital fibroblasts (OFs), and the proliferation and differentiation of OFs and lymphocytes. Activated OFs secrete inflammatory regulators, growth factors, and chemokines, thereby maintaining and amplifying the immune responses. The interactions between OFs and lymphocytes lead to the expansion and the remodeling of the orbital tissues, presenting the clinical manifestations of TAO. This review will focus on the role of T cell subsets (Type 1, Type 2, Type 17 helper T cells, and regulatory T cells) in the pathogenesis of TAO. However, we still need further studies to unravel the pathogenesis, to confirm current hypotheses, and to provide novel ideas for appropriate clinical treatment of TAO.
Highlights
Graves’ orbitopathy (GO), named after its being the most common extrathyroidal complication of Graves’ disease (GD), known as thyroid-associated ophthalmopathy (TAO) [1, 2], is an autoimmune disorder, which is found in 25–50% patients with GD, 2% patients with chronic thyroiditis, and some euthyroid cases [3]
A large amount of IL-17A was detected in the tears of TAO patients [48, 49]. These results indicated that the CD4+ Th17 cells may contribute to the immunopathological process of TAO
Due to the difficulty in obtaining orbital connective tissue specimens of early or active TAO patients without immunomodulation therapy and the lack of stable TAO animal models, the analysis of T cells infiltrating the retrobulbar tissues is usually performed using the specimens from longstanding TAO patients or patients who have experienced multiple treatments
Summary
Graves’ orbitopathy (GO), named after its being the most common extrathyroidal complication of Graves’ disease (GD), known as thyroid-associated ophthalmopathy (TAO) [1, 2], is an autoimmune disorder, which is found in 25–50% patients with GD, 2% patients with chronic thyroiditis, and some euthyroid cases [3]. CCL2 and IL-8 are potent monocyte chemotactic factors that enhance the infiltration of monocytes into orbital connective tissues of TAO patients Other cytokines such as TNF-α and growth factors such as platelet-derived growth factor (PDGF)-AA, PDGF-AB, and PDGF-AC stimulate OFs to express CCL2, CCL5, CCL7, IL-6, IL-8 and IL-16,which are involved in the recruitment and activation of T cells, B cells, and mast cells [15]. Et al demonstrated that the proportion of Treg cells in the peripheral blood leukocytes derived from TAO patients increased after incubation with rabbit polyclonal anti-T lymphocyte globulin [67] These results indicate that the number of Treg cells may be related to the severity of inflammatory responses in TAO. Little is known about the pathogenic mechanism of CD8+ T cells in TAO
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