Abstract
Graves' disease (GD) is a common autoimmune cause of hyperthyroidism, which is eventually related to the generation of IgG antibodies stimulating the thyrotropin receptor. Clinical manifestations of the disease reflect hyperstimulation of the gland, causing thyrocyte hyperplasia (goiter) and excessive thyroid hormone synthesis (hyperthyroidism). The above clinical manifestations are preceded by still partially unraveled pathogenic actions governed by the induction of aberrant phenotype/functions of immune cells. In this review article we investigated the potential contribution of natural killer (NK) cells, based on literature analysis, to discuss the bidirectional interplay with thyroid hormones (TH) in GD progression. We analyzed cellular and molecular NK-cell associated mechanisms potentially impacting on GD, in a view of identification of the main NK-cell subset with highest immunoregulatory role.
Highlights
Daniela Gallo 1†, Eliana Piantanida 1*†, Matteo Gallazzi 2†, Luigi Bartalena 1, Maria Laura Tanda 1, Antonino Bruno 3 and Lorenzo Mortara 2*
In this review article we investigated the potential contribution of natural killer (NK)
In the new era of immunotherapy, most of the efforts are addressed to cancer, as supported by the vast literature and clinical trials [135]
Summary
Daniela Gallo 1†, Eliana Piantanida 1*†, Matteo Gallazzi 2†, Luigi Bartalena 1, Maria Laura Tanda 1, Antonino Bruno 3 and Lorenzo Mortara 2*. Specialty section: This article was submitted to Thyroid Endocrinology, a section of the journal Frontiers in Endocrinology. Graves’ disease (GD) is a common autoimmune cause of hyperthyroidism, which is eventually related to the generation of IgG antibodies stimulating the thyrotropin receptor. Clinical manifestations of the disease reflect hyperstimulation of the gland, causing thyrocyte hyperplasia (goiter) and excessive thyroid hormone synthesis (hyperthyroidism). The above clinical manifestations are preceded by still partially unraveled pathogenic actions governed by the induction of aberrant phenotype/functions of immune cells
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