Flynn S D, Nishiyama R H, Bigos S T
Department of Pathology, Yale University School of Medicine, New Haven, Connecticut.
Crit Rev Clin Lab Sci. 1988;26(1):43-95. doi: 10.3109/10408368809105889.
Autoimmune thyroiditis, most notably Hashimoto's thyroiditis, appears to be increasing in prevalence and is now more easily detected by sensitive laboratory tests and more invasive procedures such as fine needle aspiration. During the last decade, marked progress has been made in the understanding of these diseases. There is a greater awareness of the interaction between the humoral and cell-mediated arms of the immune system in autoimmune thyroiditis. Recent studies implicate a subpopulation of suppressor T lymphocytes which have an antigen-specific defect, resulting in their suboptimal interaction with the helper T lymphocytes and subsequent autoimmune manifestations. There is some evidence that thyroid epithelial cells which inappropriately express HLA-DR may enhance presentation of thyroid antigens to the immune system, possibly significant in the initiation or enhancement of the autoimmune response. The presence of various antithyroid autoantibodies allows the use of laboratory assays to confirm the clinical diagnosis and predict the results of treatment. There appears to be predisposing genetic factors in the development of autoimmune thyroiditis, with some geographical and racial differences. Environmental factors, most notably dietary intake of iodine, have also been implicated in the pathogenesis of Hashimoto's thyroiditis. Several animal models have been developed addressing such issues. Ongoing studies in the areas of postpartum thyroiditis and childhood thyroiditis are helpful in clarifying their relationship with Hashimoto's thyroiditis. Graves' disease and postpartum thyroiditis are being investigated as possible causes of postpartum depression. The association of Hashimoto's thyroiditis and carcinoma of the thyroid gland is still controversial, but its relationship with malignant lymphoma is now well accepted. Thus, although the pathogenesis of autoimmune thyroiditis remains elusive, there has been significant refinement of the clinical diagnosis, and immunological abnormalities of specific intrathyroidal lymphocytes have been identified. Hopefully, these new areas of knowledge will assist in the treatment of these diseases and in the prevention of the development of malignant lymphomas of the thyroid gland.
自身免疫性甲状腺炎,最典型的是桥本甲状腺炎,其患病率似乎在上升,现在通过敏感的实验室检测和更具侵入性的检查方法(如细针穿刺抽吸)更容易被发现。在过去十年中,对这些疾病的认识取得了显著进展。人们更加了解自身免疫性甲状腺炎中免疫系统的体液免疫和细胞介导免疫分支之间的相互作用。最近的研究表明,存在一群具有抗原特异性缺陷的抑制性T淋巴细胞,这导致它们与辅助性T淋巴细胞的相互作用不理想,进而引发自身免疫表现。有证据表明,不适当表达HLA - DR的甲状腺上皮细胞可能会增强甲状腺抗原向免疫系统的呈递,这在自身免疫反应的启动或增强中可能具有重要意义。各种抗甲状腺自身抗体的存在使得可以利用实验室检测来确诊临床诊断并预测治疗结果。自身免疫性甲状腺炎的发生似乎存在易感遗传因素,并且存在一些地理和种族差异。环境因素,最显著的是碘的饮食摄入,也被认为与桥本甲状腺炎的发病机制有关。已经建立了几种针对此类问题的动物模型。正在进行的关于产后甲状腺炎和儿童甲状腺炎的研究有助于阐明它们与桥本甲状腺炎的关系。格雷夫斯病和产后甲状腺炎正在被研究是否可能是产后抑郁症的病因。桥本甲状腺炎与甲状腺癌的关联仍存在争议,但它与恶性淋巴瘤的关系现在已被广泛接受。因此,尽管自身免疫性甲状腺炎的发病机制仍然难以捉摸,但临床诊断已有显著改进,并且已经确定了甲状腺内特定淋巴细胞的免疫异常。希望这些新的知识领域将有助于治疗这些疾病并预防甲状腺恶性淋巴瘤的发生。