Milo Tomer, Korem Kohanim Yael, Toledano Yoel, Alon Uri
Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, 76100, Israel.
Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Trends Immunol. 2023 May;44(5):365-371. doi: 10.1016/j.it.2023.03.007. Epub 2023 Apr 13.
Graves' disease (GD) and Hashimoto's thyroiditis (HT) are common autoimmune diseases of the thyroid gland, causing hyperthyroidism and hypothyroidism, respectively. Despite their opposing clinical manifestation, they have several enigmatic links. Here, we propose that GD and HT have the same fundamental origin: both diseases are the cost of a beneficial physiological process called autoimmune surveillance of hypersecreting mutants. Autoreactive T cells selectively eliminate mutant cells that hypersecrete the hormones and threaten to become toxic nodules. These T cells can trigger a humoral response in susceptible individuals, leading to the production of antibodies against thyroid antigens. This shared origin can explain similarities in incidence and risk factors between HT and GD, despite their opposite clinical phenotypes.
格雷夫斯病（GD）和桥本甲状腺炎（HT）是甲状腺常见的自身免疫性疾病，分别导致甲状腺功能亢进和甲状腺功能减退。尽管它们临床表现相反，但存在一些神秘的联系。在此，我们提出GD和HT有相同的根本起源：这两种疾病都是一种名为对分泌过多突变体进行自身免疫监视的有益生理过程的代价。自身反应性T细胞选择性地清除过度分泌激素并有可能变成毒性结节的突变细胞。这些T细胞可在易感个体中引发体液反应，导致产生针对甲状腺抗原的抗体。尽管HT和GD临床表型相反，但这种共同起源可以解释它们在发病率和风险因素方面的相似性。
