Del Prete G F, Tiri A, Mariotti S, Parronchi P, Pinchera A, Romagnani S, Ricci M
Allergology and Clinical Immunology, University of Florence, Italy.
Clin Exp Rheumatol. 1989 Sep-Oct;7 Suppl 3:S41-6.
In the last few years a great deal of information on the etiopathogenetic aspects of organ-specific autoimmune diseases has been obtained from the extensive study of both animal models of experimental or spontaneous thyroiditis and of human thyroid autoimmune diseases. It has been clearly shown that genetic factors play a fundamental etiologic role. They are responsible for the dysregulation of the immune system and for the target organ susceptibility which favor the onset of the disease. Environmental factors are presumed to act as initiating or precipitating events, leading genetically predisposed individuals to thyroid autoimmunity. A number of immune mechanisms able to trigger autoimmune responses, such as antigenic cross-reactions and the aberrant expression of HLA class II molecules, have been suggested, but the definition of why and how they become operative requires further investigation. Data obtained from experimental models and from human thyroid diseases clearly indicate that the ongoing expansion of autoreactive T cells with specificity for thyroid autoantigens represents the main immunological event responsible for induction and maintenance of thyroid damage. Such autoreactive T cells can induce tissue lesions through activation of different effector systems and secretion of different combinations of lymphokines. In overt thyroid autoimmune diseases autoantibodies directed against functional molecules or cellular receptors can also be involved in the pathogenesis of tissue lesions. However, the pathogenesis of inflammatory destructive lesions of the thyroid is more complex and not yet fully elucidated. It is worthy of note that a large proportion of T cells present in inflammatory human thyroid infiltrates are apparently not directed against the thyroid autoantigens recognized so far.(ABSTRACT TRUNCATED AT 250 WORDS)
在过去几年中，通过对实验性或自发性甲状腺炎的动物模型以及人类甲状腺自身免疫性疾病的广泛研究，已经获得了大量关于器官特异性自身免疫性疾病病因发病机制方面的信息。已经清楚地表明，遗传因素起着基本的病因学作用。它们导致免疫系统失调以及靶器官易感性增加，从而有利于疾病的发生。环境因素被认为是引发或促成疾病的事件，使具有遗传易感性的个体发生甲状腺自身免疫。已经提出了一些能够引发自身免疫反应的免疫机制，如抗原交叉反应和HLA II类分子的异常表达，但对于它们为何以及如何起作用的定义仍需要进一步研究。从实验模型和人类甲状腺疾病中获得的数据清楚地表明，针对甲状腺自身抗原具有特异性的自身反应性T细胞的持续扩增是导致甲状腺损伤诱导和维持的主要免疫事件。这种自身反应性T细胞可通过激活不同的效应系统和分泌不同组合的淋巴因子来诱导组织损伤。在明显的甲状腺自身免疫性疾病中，针对功能分子或细胞受体的自身抗体也可能参与组织损伤的发病机制。然而，甲状腺炎性破坏性病变的发病机制更为复杂，尚未完全阐明。值得注意的是，在人类甲状腺炎性浸润中存在的很大一部分T细胞显然并非针对目前已识别的甲状腺自身抗原。（摘要截短于250字）
