Kawana S, Geoghegan W D, Jordon R E
Clin Exp Immunol. 1985 Sep;61(3):517-25.
We have previously demonstrated that pemphigus antibodies will fix complement to organ and tissue cultured epidermal cells in vitro. In the present study, we sought to determine the role complement plays in the detachment of cultured murine epidermal cells by pemphigus antibody. Forty-eight hour cultivated epidermal monolayers from neonatal BALB/c mice were treated with purified IgG fractions of pemphigus sera in the presence or absence of complement. In the absence of complement, pemphigus IgG produced slight cell detachment when compared to an identical amount of normal IgG. When cells were maintained in media with pemphigus IgG plus complement for 48 h, the cell detachment was significantly higher than that obtained with pemphigus IgG alone, or with normal IgG plus complement. Heat inactivation or Clq depletion of the complement source resulted in complete inhibition of cell detachment. When pemphigus F(ab')2 plus complement was used instead of whole pemphigus IgG plus complement, the cell detachment rate was again lowered significantly. Both pemphigus IgG and the complement source were depleted of plasminogen by passage over a lysine-Sepharose 4B column, and tested for their effects on cell detachment depleted of plasminogen. Depletion of plasminogen failed to inhibit cell detachment induced by pemphigus IgG and complement. These results suggest that complement activated by pemphigus antibody binding to the epidermal cell surface induces epidermal cell detachment and would argue against the plasminogen-plasmin system as the sole cause of cell detachment in pemphigus.
我们之前已经证明,天疱疮抗体在体外可使补体结合到器官和组织培养的表皮细胞上。在本研究中,我们试图确定补体在天疱疮抗体诱导培养的小鼠表皮细胞脱离过程中所起的作用。用天疱疮血清的纯化IgG组分处理来自新生BALB/c小鼠的培养48小时的表皮单层细胞,处理时存在或不存在补体。在不存在补体的情况下,与等量的正常IgG相比,天疱疮IgG产生轻微的细胞脱离。当细胞在含有天疱疮IgG加补体的培养基中维持48小时时,细胞脱离明显高于单独使用天疱疮IgG或正常IgG加补体时的情况。补体来源的热灭活或Clq缺失导致细胞脱离完全受到抑制。当使用天疱疮F(ab')2加补体代替完整的天疱疮IgG加补体时,细胞脱离率再次显著降低。天疱疮IgG和补体来源都通过赖氨酸-琼脂糖4B柱去除纤溶酶原,并测试它们对去除纤溶酶原的细胞脱离的影响。去除纤溶酶原未能抑制天疱疮IgG和补体诱导的细胞脱离。这些结果表明,天疱疮抗体与表皮细胞表面结合激活的补体诱导表皮细胞脱离,这表明纤溶酶原-纤溶酶系统并非天疱疮中细胞脱离的唯一原因。