Wallace W A, Howie S E
Department of Pathology, Edinburgh University Medical School, Edinburgh, EH8 9AG, UK.
J Pathol. 2001 Sep;195(2):251-6. doi: 10.1002/path.916.
Type II alveolar epithelial cells express a 70-90 kDa antigen to which circulating auto-antibodies have been previously identified in patients with cryptogenic fibrosing alveolitis (CFA). In vitro experiments have been conducted with a rabbit polyclonal antibody raised to this auto-antigen, and the type II epithelial cell line A549. This study examined possible effects that interaction of this antibody with type II epithelial cells might have on the production of cytokines and extracellular matrix components that may be important in the pathogenesis of CFA. There was a significant increase in TGFbeta and tenascin, but not IL4, production by the A549 cells after culture with the immune serum. Further experiments showed that after 72 hours in culture, the antibody decreased A549 cell number in a complement-dependent process, which appeared to be cytostatic rather than cytolytic. These results indicate in vitro biological activity for this antibody and suggest a possible in vivo role for auto-antibody to type II epithelial cells in the pathogenesis of CFA.
II型肺泡上皮细胞表达一种70 - 90 kDa的抗原,在隐源性纤维性肺泡炎(CFA)患者中,先前已鉴定出针对该抗原的循环自身抗体。已使用针对这种自身抗原产生的兔多克隆抗体和II型上皮细胞系A549进行了体外实验。本研究检测了该抗体与II型上皮细胞相互作用可能对细胞因子和细胞外基质成分产生的影响,这些成分在CFA的发病机制中可能很重要。用免疫血清培养后,A549细胞产生的转化生长因子β(TGFbeta)和腱生蛋白显著增加,但白细胞介素4(IL4)没有增加。进一步的实验表明,培养72小时后,该抗体在补体依赖的过程中减少了A549细胞数量,这似乎是细胞抑制而非细胞溶解。这些结果表明该抗体具有体外生物学活性,并提示自身抗体对II型上皮细胞在CFA发病机制中可能具有体内作用。