HIT_4单抗对金黄色葡萄球菌CowanⅠ菌体诱导IgG分泌的抑制效应  

Inhibitory Effect of HIT_4. McAb on IgG Synthesis

作　　者：杨春瑛[1] 沈德诚[1] 程庆年 张金香[1] 杨希峰[1] 苏月来[1] 孙同哲[1] 

机构地区：[1]中国医学科学院血液学研究所

出　　处：《上海免疫学杂志》1995年第1期4-6,共3页Shanghai Journal of Immunology

基　　金：国家自然科学基金

摘　　要：本文报道了ＨＩＴ４单抗对金黄色葡萄球菌ＣｏｗａｎⅠ菌体（ＳＡＣ）诱导的ＩｇＧ分泌的抑制效应．研究发现ＨＩＴ４单抗可明显抑制ＳＡＣ诱导的正常人和ＩＴＰ患者外周血单个核细胞（ＰＢＭＣ）分泌ＩｇＧ，平均抑制率分别为８１．４±１２．０％和９２．７±１２．８％，而对Ｉｇ分泌水平低下的新生儿脐血单个核细胞无调节作用。ＨＩＴ４单抗的抑制作用是通过ＨＩＴ４＋细胞表面ＨＩＴ４抗原特异性介导，选择地作用于ＳＡＣ（而不是ＰＷＭ）诱导的ＩｇＧ分泌过程，具有剂量依赖性。本研究为了解ＨＩＴ４单抗的生物学特点及可能具有的临床应用前景提供了资料。The inhibitory effect of HIT. McAb on SAC mitogen-driven IgG synthesis of peripheral blood lymphocytes has been studied. The result demonstrated that HIT4 McAb could strongly inhibit IgG synthesis induced by SAC mitogen. The mean inhibitory rates were 81. 4±12.0% and 92. 7±12. 8% in normal donors and ITP patients respectively. But no inhibition was observed in cord blood lymphocytes which showed low-level synthesis of IgG. We further investigated the mechanism of the inhibitory activity. The result indicated that the inhibitory activity was dose-dependent, mediated specifically via HIT4 surface antigen and might affect on the stage of B cell activation induced by SAC mitogen. We also found that the resting HIT4 cells could exert the inhibitory function only after activated by HIT4 McAb. This study provided useful data for understanding the biological properties and clinical potentiality of HIT4 McAb.

关 键 词：单克隆抗体 IgG分泌 金黄葡萄球菌 

分 类 号：R392.11[医药卫生—免疫学]