Abstract
There is now considerable evidence that T cell-mediated immunity plays a major role in the pathogenesis of thyroid-associated ophthalmopathy. Circulating T cell phenotypes are altered and subtle markers of T cell activation are raised in active disease. Such T cells can also be stimulated by orbital autoantigens, although the responses are generally weak and the nature of the autoantigen is unclear. Immunohistochemical and molecular studies have shown that activated T cells accumulate in the retrobulbar tissue and release cytokines which preferentially activate local fibroblasts. T cell lines have been derived from the retrobulbar tissue which recognise fibroblast autoantigens. Together, these results are compatible with a model for disease pathogenesis in which the interaction between T cells and fibroblasts leads to extraocular muscle swelling and the clinical features of ophthalmopathy.