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为探讨Ｇｒａｖｅｓ眼病（ＧＯ）的发病机理，我们对新近发现的眼肌自身抗原及存在于ＧＯ患者血清的眼肌抗体进行了研究。血清取自１８例正常人、１８例活动性ＧＯ、１０例无限征的Ｇｒａｖｅｓ甲亢（ＧＨ）和３例桥本甲状腺炎（ＨＴ）患者。人眼肌膜蛋白经ＧＯ患者混合ＩｇＧ亲和层析后进行ＳＤＳ－聚丙烯酰胺凝胶电泳，显示分子量为４５、２８、５５和６４ｋＤ等蛋白条带。经正常人混合ＩｇＧ亲和层析未能显示上述结果。Ｗｅｓｔｅｒｎ印迹杂交虽然未能证实仅与患者血清作用的独特的眼肌抗原的存在，但６４ｋＤ印迹存在于６１％的ＧＯ、３０％的ＧＨ、０％的ＨＴ患者，正常人仅２２％阳性。抗６４ｋＤ阳性率ＧＯ组明显高于对照组（Ｐ＜０．０５）。眼肌抗体（ＥＭＡｂ）特别是抗６４ｋＤ抗体对于ＧＯ发病机理的作用值得进一步研究。
In order to explore the pathogenesis of Graves ophthalmopathy (GO), we studied newly discovered ocular autoantigens and ocular antibodies present in serum of GO patients. Serum samples were taken from 18 normal subjects, 18 active GO patients, 10 non-limited Graves hyperthyroidism (GH) and 3 Hashimoto’s thyroiditis (HT) patients. Human ocular muscle protein by GO patients mixed with IgG affinity chromatography after SDS-polyacrylamide gel electrophoresis showed that the molecular weight of 45,28,55 and 64kD and other protein bands. The results of normal human IgG hybridization failed to show the above results. While Western blotting did not confirm the existence of a unique ocular antigens that only interacted with patient sera, the 64kD blots were present in 61% of GO, 30% of GH, and 0% of HT patients, with only 22% of normal subjects positive. The anti-64kD positive rate in GO group was significantly higher than that in control group (P <0.05). The role of ocular muscle antibodies (EMAb), especially anti-64 kD antibodies, on the pathogenesis of GO deserves further study.