Natt N, Bahn R S
Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, MN 55905, USA.
Autoimmunity. 1997;26(2):129-36. doi: 10.3109/08916939709003857.
Infiltration of the retroocular space by inflammatory cells and the accumulation of glycosaminoglycans are histological characteristics of Graves' ophthalmopathy. Various cytokines, released by infiltrating immunocompetent cells and resident connective tissue cells, play a pivotal role in the evolution of this disease. The predominant cytokines secreted by orbital T cells during the course of the disease may govern the activity and stage of the local autoimmune process. Cytokine effects of potential relevance to the pathogenesis of Graves' ophthalmopathy include their ability to stimulate orbital fibroblasts to proliferate and secrete excess quantities of glycosaminoglycans. The edema associated with these hydrophilic macromolecules is directly responsible for many of the characteristic clinical features of the disease. In addition, certain cytokines induce or enhance the expression on orbital fibroblasts of immunomodulatory proteins. We review current evidence supporting the notion that cytokines are central to the development and evolution of Graves' ophthalmopathy.
炎性细胞浸润眼球后间隙以及糖胺聚糖的积聚是格雷夫斯眼病的组织学特征。浸润的免疫活性细胞和驻留的结缔组织细胞释放的各种细胞因子在该疾病的发展过程中起关键作用。疾病过程中眼眶T细胞分泌的主要细胞因子可能控制局部自身免疫过程的活动和阶段。与格雷夫斯眼病发病机制潜在相关的细胞因子作用包括它们刺激眼眶成纤维细胞增殖并分泌过量糖胺聚糖的能力。与这些亲水性大分子相关的水肿直接导致了该疾病许多典型的临床特征。此外，某些细胞因子诱导或增强眼眶成纤维细胞上免疫调节蛋白的表达。我们综述了支持细胞因子是格雷夫斯眼病发生和发展核心这一观点的现有证据。
