Langlois A J, Matthews T, Roloson G J, Thiel H J, Collins J J, Bolognesi D P
J Immunol. 1981 Jun;126(6):2337-41.
An in vitro assay has been developed that mimics the potent in vivo protective capacity of B6 anti-AD755a serum in a passive therapy protocol. In the presence of small volumes of hyperimmune serum or IgG2a antibody, thioglycollate-elicited B6 mouse peritoneal cells (PEC) inhibit the growth of AD755 Cl.10 target cells and other cells provided that they express FLV-related antigens. When hyperimmune serum is replaced by normal serum, or elicited PEC from BALB/c mice are used, growth inhibition of the AD755 Cl.10 target cells is not seen. The latter is in accord with the inability to protect BALB/c mice with the anti-AD755a serum. Tumor cells to which antibody has been pre-bound are not inhibited by thioglycollate-elicited B6 PEC, analogous to the undiminished tumorigenicity of antibody-bound AD755a cells in vivo. These results, along with those presented in the accompanying papers, have led to the construction of a model to explain the specificity and mechanism of the potent in vivo passive protection characteristic of this system. The major features of this model are that the protective IgG2a antibody must first interact with an appropriate host effector cell, presumably of the monocyte/macrophage lineage, and that such an antibody-directed cell then binds to the tumor cell and effects its elimination, possibly by a phagocytic mechanism.
已开发出一种体外试验,该试验模拟了B6抗AD755a血清在被动治疗方案中强大的体内保护能力。在存在少量超免疫血清或IgG2a抗体的情况下,经巯基乙酸盐诱导的B6小鼠腹腔细胞(PEC)可抑制AD755 Cl.10靶细胞及其他表达FLV相关抗原的细胞的生长。当用正常血清替代超免疫血清,或使用来自BALB/c小鼠的诱导PEC时,则看不到对AD755 Cl.10靶细胞的生长抑制。后者与抗AD755a血清无法保护BALB/c小鼠一致。预先结合了抗体的肿瘤细胞不会被经巯基乙酸盐诱导的B6 PEC抑制,这类似于体内抗体结合的AD755a细胞未减弱的致瘤性。这些结果,连同随附论文中呈现的结果,已促成构建一个模型,以解释该系统强大的体内被动保护特性的特异性和机制。该模型的主要特征是,保护性IgG2a抗体必须首先与适当的宿主效应细胞相互作用,推测该细胞为单核细胞/巨噬细胞谱系,并且这种抗体导向的细胞随后与肿瘤细胞结合并通过吞噬机制等作用将其清除。