Weidner F
Arch Dermatol Res (1975). 1975 Oct 29;253(3):249-59. doi: 10.1007/BF00561151.
Using an indirect double layer immunofluorescence method, fresh skin lesions of 10 patients with different forms of cutaneous vasculitis were tested for the occurrence of complement-factors C1q (C1), alpha2D(C3) and beta1F (C5). In contrast to the irregularly found complement fixing immunoglobulins IgG and IgM, complement could be regularly seen bound to the cutaneous vessel walls; mostly the C3-factor alpha2D. C1q was demonstrable, combined with IgG and/or IgM only in 2 cases. In 5 patients there was a non-homogenous, roddy fluorescenece of the epidermal basal membrane zone and the cutaneous vessels, when alpha2D or beta1F were tested. Our findings suggest that the "alternate pathway" beginning with C3-activation is followed in most cases, whereas a typical "immune complex vasculitis" is obviously rare. The constant occurrence of complement in the cutaneous vessel walls of vascultis lesions is consistent with the known chemotactic and destructive role of complement factors in experimental models of angiitis, but it may not necessarily involve a specific immunological process.
采用间接双层免疫荧光法,对10例不同类型皮肤血管炎患者的新鲜皮肤损害进行补体因子C1q(C1)、α2D(C3)和β1F(C5)检测。与补体结合免疫球蛋白IgG和IgM的不规则发现不同,补体可经常在皮肤血管壁上见到;多数为C3因子α2D。仅在2例中可证实C1q与IgG和/或IgM结合。检测α2D或β1F时,5例患者的表皮基底膜区和皮肤血管出现非均一性、条索状荧光。我们的研究结果提示,多数情况下遵循始于C3激活的“替代途径”,而典型的“免疫复合物性血管炎”显然少见。补体在血管炎损害的皮肤血管壁中持续存在,这与补体因子在血管炎实验模型中已知的趋化和破坏作用相符,但不一定涉及特定的免疫过程。