Muraguchi A, Kishimoto T, Kuritani T, Yamamura Y
J Immunol. 1980 Dec;125(6):2638-42.
Effect of anti-mu and anti-delta antibodies on PHA- and protein A-induced B colony formation was studied. Anti-mu antibody at any concentrations tested did not show inhibitory or enhancing effect on colony formation. On the other hand, anti-delta antibody enhanced both PHA- and protein A-induced colony formation. Optimum concentration of anti-delta antibody for maximum enhancement was 0.1 microgram/ml. and F(ab')2 fragment of anti-delta antibody also showed comparable enhancing effect. Simultaneous addition of IgD with anti-delta antibody abrogated anti-delta-induced enhancement, and anti-delta antibody did not show any facilitation of colony formation in IgM+ IgD- cell population. In marked contrast with normal B cells, anti-mu antibody showed a remarkable enhancing effect on protein A-induced colony formation of B cells from JRA patients. F(ab')2 fragment of anti-mu antibody also showed comparable enhancing effect. Anti-mu antibody did not show any enhancement of colony formation of B cells from several other autoimmune diseases. The result indicated the presence of abnormal B cells in JRA patients.
研究了抗μ和抗δ抗体对PHA和蛋白A诱导的B细胞集落形成的影响。在所测试的任何浓度下,抗μ抗体对集落形成均未显示出抑制或增强作用。另一方面,抗δ抗体增强了PHA和蛋白A诱导的集落形成。抗δ抗体最大增强作用的最佳浓度为0.1微克/毫升,抗δ抗体的F(ab')2片段也显示出相当的增强作用。将IgD与抗δ抗体同时添加可消除抗δ诱导的增强作用,并且抗δ抗体在IgM+IgD-细胞群体中未显示出对集落形成的任何促进作用。与正常B细胞形成鲜明对比的是,抗μ抗体对幼年类风湿性关节炎(JRA)患者B细胞的蛋白A诱导的集落形成显示出显著的增强作用。抗μ抗体的F(ab')2片段也显示出相当的增强作用。抗μ抗体对其他几种自身免疫性疾病患者的B细胞集落形成未显示出任何增强作用。结果表明JRA患者中存在异常B细胞。