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目的 探讨９．１Ｃ３分子对ＣＤ２和ＣＤ３诱导的ＰＢＭＣ杀伤作用的影响及其作用机制。方法以活化ＰＢＭＣ为效应细胞，采用重导向杀伤实验（ｒｅｄｉｒｅｃｔｅｄ ｃｙｔｏｔｏｘｉｃｉｔｙ ａｓｓａｙ，ＲＣＡ），观察９．１Ｃ３对ＣＤ２、ＣＤ３介导效应细胞杀伤Ｐ８１５细胞作用的影响。以Ｊｕｒｋａｔ细胞为模型，用相应的抗体刺激细胞，通过荧光分光光度计，测定９．１Ｃ３对ＣＤ２、ＣＤ３诱导［Ｃａ２＋］ｉ升高的影响。结果９．１Ｃ３ ｍＡｂ能显著抑制ＣＤ２ ｍＡｂ介导活化ＰＢＭＣ对Ｐ８１５细胞的杀伤作用，但对ＣＤ３ ｍＡｂ介导杀伤的抑制作用较弱。以Ｊｕｒｋａｔ细胞为模型，发现ＣＤ２ ｍＡｂ经羊抗鼠Ｉｇ（ｇｏａｔ ａｎｔｉ ｍｏｕｓｅ Ｉｇ， ＧＡＭ Ｉｇ）交联后能诱导［Ｃａ２＋］ｉ的升高，当同时加入９．１Ｃ３ ｍＡｂ时，［Ｃａ２＋］ｉ的升高受到抑制；ＣＤ３ ｍＡｂ在没有ＧＡＭ Ｉｇ交联时即能引起［Ｃａ２＋］ｉ的升高，而９．１Ｃ３ ｍＡｂ对ＣＤ３ ｍＡｂ诱导［Ｃａ２＋］ｉ的升高有赖于ＧＡＭ Ｉｇ的交联。结论９．１Ｃ３分子对ＣＤ２和ＣＤ３介导的杀伤的抑制程度不同。抑制杀伤细胞脱颗粒依赖的［Ｃａ２＋］ｉ升高可能是９．１Ｃ３分子抑制活?
Objective To investigate the effect of 9.1C3 on CD2 and CD3-induced PBMC killing and its mechanism. Methods The PBMC was taken as effector cells and the effect of 9.1C3 on CD2 and CD3-mediated killing of P815 cells was observed by using redirected cytotoxicity assay (RCA). Using Jurkat cells as a model, cells were stimulated with the corresponding antibodies and the effect of 9.1C3 on [CD2 +, CD3-induced [Ca2 +] i elevation was measured by a fluorescence spectrophotometer. Results 9.1C3 mAb could significantly inhibit CD2 mAb-mediated cytotoxicity of activated PBMCs on P815 cells, but its inhibitory effect on CD3 mAb-mediated killing was weak. Using Jurkat cells as a model, we found that CD2 mAb induced the increase of [Ca2 +] i after cross-linking with goat anti-mouse Ig (GAM Ig). When adding 9.1C3 mAb, Elevated inhibition was suppressed; CD3 mAb caused an increase in [Ca2 +] i in the absence of GAM Ig cross-linking, whereas 9.1C3 mAb induced a CD3 mAb-induced increase in [Ca2 +] i dependent on cross-linking of GAM Ig. Conclusion 9.1C3 molecules inhibit CD2 and CD3-mediated cytotoxicity differently. Inhibition of killer cell degranulation-dependent increase of [Ca2 +] i may be 9.1C3 molecule inhibition activity?