生物
长时程增强
细胞
抗体
B细胞
分子生物学
单克隆抗体
淋巴细胞
免疫学
细胞毒性
受体
生物化学
体外
作者
Mikael Jondal,Charlotte Kullman,Maj-Britt Alter,K Ljunggren
标识
DOI:10.1016/0008-8749(86)90016-x
摘要
Pretreatment of normal human lymphocytes with monoclonal IgG against the NK cell-FcR (IgG) or the T3 complex was found to potentiate killing of most NK sensitive target cells with the exception of T-cell derived cells. Anti-FcR IgM monoclonals were suppressive for all target cells. IgG anti-FcR mediated potentiation required minute amounts of antibody but was also seen at high anti-FcR concentrations that modulated FcR activity. Potentiated and FcR modulated cells retained anti-FcR IgG on the membrane and conjugated normally to target cells. Anti-FcR potentiation blocked antibody-dependent killing but did not influence lectin-dependent killing, with anti-T3 the opposed effect was seen. Combined anti-FcR and anti-T3 treatment resulted in decreased potentiation. The results suggest that the NK cell-FcR may be activated during normal NK cell killing (without the addition of antibody) as suggested for FcR in B cell triggering.
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