Tandon N, Morgan B P, Weetman A P
Department of Medicine, University of Sheffield Clinical Sciences Centre, Northern General Hospital, U.K.
Immunology. 1992 Feb;75(2):372-7.
Human thyroid cells are resistant to lysis by the homologous membrane attack complex. By immunohistochemical staining we here show that normal thyroid cells and those in Graves' disease and Hashimoto's thyroiditis express two membrane attack complex-inhibiting proteins, CD59 antigen and membrane attack complex-inhibiting protein/homologous restriction factor (MIP/HRF). In vitro, the expression of both molecules was enhanced by interleukin-1 (IL-1), tumour necrosis factor (TNF) and interferon-gamma (IFN-gamma) and cytokine-treated thyroid cells were more resistant to lysis by homologous complement. Blocking experiments with monoclonal antibodies against CD59 antigen and MIP/HRF showed that both molecules contributed but CD59 antigen was the more important in mediating resistance to complement attack. Expression of these proteins may be an important determinant of the severity of tissue injury produced by complement-fixing thyroid peroxidase antibodies in autoimmune thyroid disease.
人甲状腺细胞对同源膜攻击复合物介导的细胞溶解具有抗性。通过免疫组织化学染色,我们在此表明,正常甲状腺细胞以及格雷夫斯病和桥本甲状腺炎中的甲状腺细胞表达两种膜攻击复合物抑制蛋白,即CD59抗原和膜攻击复合物抑制蛋白/同源限制因子(MIP/HRF)。在体外,白细胞介素-1(IL-1)、肿瘤坏死因子(TNF)和干扰素-γ(IFN-γ)可增强这两种分子的表达,且经细胞因子处理的甲状腺细胞对同源补体介导的细胞溶解更具抗性。用抗CD59抗原和MIP/HRF的单克隆抗体进行的阻断实验表明,这两种分子均发挥作用,但CD59抗原在介导对补体攻击的抗性方面更为重要。这些蛋白的表达可能是自身免疫性甲状腺疾病中补体结合性甲状腺过氧化物酶抗体所产生的组织损伤严重程度的重要决定因素。