Hong K, Kinoshita T, Kitajima H, Inoue K
J Immunol. 1981 Jul;127(1):104-8.
K-76COOH caused dose-dependent inhibition of the degradation, by C3b inactivator (C3bINA) and beta 1H, of membrane-bound C3b on EAC1-3b and of free C3b in the fluid phase, i.e., cleavage of the C3b alpha' peptide chain. K-76COOH primarily attacked C3bINA but not beta 1H or C3b. K-76COOH inhibited the suppression of immune adherence reactivity and the manifestation of conglutination reactivity of EAC1-3b cells by C3bINA and beta 1H. The drug also inhibited the reaction between conglutinin and EAC1-3b' cells derived from EAC1-3b by treatment with C3bINA and beta 1H. EAC1-3b cells did not form rosettes with either Daudi or Raji lymphoblastoid cells. Treatment with C3bINA and beta 1H rendered EAC1-3b cells reactive with Daudi cells, and this change was inhibited by K-76COOH. EAC1-3b cells became able to form rosettes with Raji cells after addition of beta 1H. This rosette formation was enhanced by further addition of C3bINA, and this enhancement was also suppressed by K-76COOH.
K-76COOH对补体C3b灭活因子（C3bINA）和β1H介导的EAC1-3b上膜结合C3b及液相中游离C3b的降解具有剂量依赖性抑制作用，即C3bα'肽链的裂解。K-76COOH主要作用于C3bINA，而非β1H或C3b。K-76COOH抑制了C3bINA和β1H对EAC1-3b细胞免疫黏附反应性的抑制作用以及共凝集反应性的表现。该药物还抑制了共凝集素与经C3bINA和β1H处理后从EAC1-3b衍生而来的EAC1-3b'细胞之间的反应。EAC1-3b细胞与Daudi或Raji淋巴母细胞均不形成花环。用C3bINA和β1H处理使EAC1-3b细胞与Daudi细胞发生反应，而这种变化受到K-76COOH的抑制。加入β1H后，EAC1-3b细胞能够与Raji细胞形成花环。进一步加入C3bINA可增强这种花环形成，而这种增强也受到K-76COOH的抑制。
