Newman S, Glovsky M M, Ghekiere L, Alenty A
J Allergy Clin Immunol. 1977 Apr;59(4):327-33. doi: 10.1016/0091-6749(77)90055-0.
The requirements of complement (C) to induce systemic and cutaneous Forssman reactions were studied in inbred DHC-BA and Hartley strain guinea pigs. After intravenous injection of Forssman antibody, fatal systemic shock was associated with a marked drop in CH50, C4, and C3 and a lesser decrease in C5 hemolytic activity. Platelet counts and leukocyte counts dropped as well. With the use of the purified low molecular weight factor from cobra venom (CVF) to deplete C3, guinea pigs with less than 1% intravascular C3 were protected from lethal shock. Approximately 1% to 3% C3 activity is required for Forssman cutaneous vasculitis. These results confirm earlier studies that classical complement pathway activation occurs in Forssman shock and demonstrate the exquisite biologic efficiency of C3 in provoking the shock syndrome.
在近交系DHC - BA和Hartley品系豚鼠中研究了补体(C)诱导全身性和皮肤福斯曼反应的条件。静脉注射福斯曼抗体后,致命性全身休克与CH50、C4和C3显著下降以及C5溶血活性较小程度降低相关。血小板计数和白细胞计数也下降。使用从眼镜蛇毒(CVF)中纯化的低分子量因子耗尽C3后,血管内C3低于1%的豚鼠可免受致命性休克。福斯曼皮肤血管炎需要大约1%至3%的C3活性。这些结果证实了早期的研究,即经典补体途径激活发生在福斯曼休克中,并证明了C3在引发休克综合征方面具有极高的生物学效率。