Nakai H, Hirakawa S, Hayakawa N, Amano T, Ota Z
Third Department of Internal Medicine, Okayama University Medical School, Japan.
Acta Med Okayama. 1992 Oct;46(5):323-30. doi: 10.18926/AMO/32658.
Cytotoxic anti-thyroid microsomal autoantibodies are highly prevalent in sera of patients with Graves' disease, but in Graves' disease thyroid tissues rarely show destructive changes. We postulated that this might be due to membrane-associated complement regulatory proteins which protect target cells from injury by complement activation. We, therefore, investigated the expression of membrane attack complex inhibitory factor (MACIF) and decay accelerating factor (DAF) in the thyroid tissues from patients with Graves' disease, Hashimoto's thyroiditis, thyroid adenocarcinoma and normal human thyroid tissues. We found a high level of expression of MACIF and DAF in Graves' thyroid tissues. Using the membrane immunofluorescence and cell-ELISA techniques, we also investigated the factors which enhanced the MACIF and DAF expression in cultured thyroid cells. Thyroid stimulating hormone, phorbol 12, 13-dibutyrate and thyroid stimulating autoantibody enhanced the MACIF and DAF expression. These findings suggest that the membrane complement regulatory proteins increase in response to the thyroid stimulating factors such as thyroid stimulating autoantibody in Graves' disease and that this increase then protects the cells from damage due to complement activation by thyroid autoantibodies.
细胞毒性抗甲状腺微粒体自身抗体在格雷夫斯病患者血清中高度流行,但在格雷夫斯病中,甲状腺组织很少出现破坏性变化。我们推测这可能是由于膜相关补体调节蛋白保护靶细胞免受补体激活损伤所致。因此,我们研究了膜攻击复合物抑制因子(MACIF)和衰变加速因子(DAF)在格雷夫斯病、桥本甲状腺炎、甲状腺腺癌患者的甲状腺组织以及正常人体甲状腺组织中的表达。我们发现MACIF和DAF在格雷夫斯病甲状腺组织中高表达。利用膜免疫荧光和细胞酶联免疫吸附测定技术,我们还研究了在培养的甲状腺细胞中增强MACIF和DAF表达的因素。促甲状腺激素、佛波醇12,13 - 二丁酸酯和促甲状腺自身抗体增强了MACIF和DAF的表达。这些发现表明,在格雷夫斯病中,膜补体调节蛋白会因促甲状腺自身抗体等促甲状腺因子的作用而增加,这种增加进而保护细胞免受甲状腺自身抗体激活补体所造成的损伤。