Caturegli Patrizio, Kimura Hiroaki, Rocchi Roberto, Rose Noel R
Department of Pathology, The Johns Hopkins School of Medicine, Baltimore, Maryland 21205, USA.
Curr Opin Rheumatol. 2007 Jan;19(1):44-8. doi: 10.1097/BOR.0b013e3280113d1a.
Interesting clinical and basic studies have been published in the field of autoimmune thyroiditis (represented by Graves' disease and Hashimoto's thyroiditis) since January 2005. The review is organized into four main areas: genetics, environment, adaptive immune system, and innate immune system.
The quest continues for the identification of susceptibility genes for autoimmune thyroiditis. In addition to the classical major histocompatibility complex class II genes and cytotoxic T cell antigen-4, new studies have appeared on CD40 the protein tyrosine phosphatase-22. Too much iodine increases the incidence of Hashimoto's thyroiditis, perhaps by augmenting the antigenicity of thyroglobulin. T regulatory cells, Toll-like receptors and presentation of lipid antigens by CD1 molecules are new areas of basic immunological investigation that have been applied to autoimmune thyroiditis.
Overall, the studies have greatly expanded our understanding of the pathogenesis of thyroiditis. They have opened new lines of investigations that will ultimately result in a better clinical practice.
自2005年1月以来，自身免疫性甲状腺炎（以格雷夫斯病和桥本甲状腺炎为代表）领域发表了一些有趣的临床和基础研究。本综述分为四个主要领域：遗传学、环境、适应性免疫系统和固有免疫系统。
对自身免疫性甲状腺炎易感基因的鉴定工作仍在继续。除了经典的主要组织相容性复合体II类基因和细胞毒性T细胞抗原4外，关于CD40和蛋白酪氨酸磷酸酶22的新研究也已出现。碘摄入过多会增加桥本甲状腺炎的发病率，可能是通过增强甲状腺球蛋白的抗原性。调节性T细胞、Toll样受体以及CD1分子对脂质抗原的呈递是基础免疫学研究的新领域，已应用于自身免疫性甲状腺炎。
总体而言，这些研究极大地扩展了我们对甲状腺炎发病机制的理解。它们开辟了新的研究方向，最终将带来更好的临床实践。
