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为鉴定介导ＮＫ细胞激活的表面分子及其作用机制，本研究用一系列粘附分子单抗及配体体外刺激ＮＫ细胞，定量检测ＮＫ细胞ＩＦＮ－γ的分泌；检测了ＮＫ细胞经ＩＬ－２诱导后其异构体的变化及其不同异构体单抗对ＮＫ细胞的刺激作用；以ＣＤ２２α、ＣＤ２２β基因导入Ｂ７８Ｈ１细胞后观察转染细胞对ＮＫ细胞的粘附和刺激效应。结果表明：ＩｇＧ２ａ和ＩｇＧ１亚类ＣＤ４５单抗及其Ｆ（ａｂ）２均可独立刺激ＮＫ细胞释放ＩＦＮ－γ；ＮＫ细胞经ＩＬ－２培养诱导后其表面ＣＤ４５分子异构体的表达呈ＲＯ逐渐增加，而ＲＡ逐渐减少的特征；ＣＤ４５ＲＯ单抗可刺激ＮＫ细胞释放ＩＦＮ－γ；ＣＤ２２α、ＣＤ２２β转染细胞可粘附，但不能刺激ＮＫ细胞激活。结果提示：ＮＫ细胞可经ＣＤ４５ＲＯ途径激活并释放ＩＦＮ－γ，该途径与ＣＤ１６分子无关，ＣＤ４５分子的特异性配体并非既往所报道的ＣＤ２２，尚待进一步鉴定
In order to identify the surface molecules that mediate NK cell activation and its mechanism of action, NK cells were stimulated with a series of adherent monoclonal antibodies and ligands in vitro to quantitatively detect the secretion of IFN-γ by NK cells. 2 after isoflurane-induced isoforms and NK cells were stimulated by different isoforms of McAbs. After transfecting B78H1 cells with CD22α and CD22β genes, the adhesion and stimulatory effects of transfected cells on NK cells were observed. The results showed that IgG2a and IgG1 subtypes CD45 monoclonal antibody and its F (ab) 2 could independently stimulate NK cells to release IFN-γ. The expression of CD45 molecular isoform on NK cells was gradually increased after IL-2 culture Increased, and RA gradually decreased; CD45RO monoclonal antibody can stimulate NK cells release IFN-γ; CD22α, CD22β transfected cells can adhere, but can not stimulate NK cell activation. The results suggest that NK cells can activate and release IFN-γ via the CD45RO pathway, which is independent of CD16. The specific ligand of CD45 is not the previously reported CD22, yet further identification