Liu Y N, Uchida T, Ju S T, Dorf M E
Cell Immunol. 1985 Apr 15;92(1):142-53. doi: 10.1016/0008-8749(85)90072-3.
Cloned macrophage hybridoma cells derived from fusions between splenic adherent cells of CKB mice and the drug-marked P388D1 cell line were studied to further understand macrophage-mediated tumoricidal activity at the clonal level. Most of the macrophage hybridomas were specifically activated by a combination of lymphokine and lipopolysaccharide (LPS), but were not activated by either agent alone. There is no apparent correlation between macrophage-mediated tumor cytotoxicity and the ability of LPS to induce interleukin 1 (IL-1) secretion or of concanavalin A (Con A) supernatants containing interferon-gamma to increase H-2 and Ia expression. Thus, one hybridoma clone which was unable to kill tumor cells was still sensitive to LPS and lymphokine activation by the latter criterion.
为了在克隆水平上进一步了解巨噬细胞介导的杀瘤活性,对从CKB小鼠脾粘附细胞与药物标记的P388D1细胞系融合得到的克隆化巨噬细胞杂交瘤细胞进行了研究。大多数巨噬细胞杂交瘤通过淋巴因子和脂多糖(LPS)的组合被特异性激活,但单独使用任何一种试剂都不能激活。巨噬细胞介导的肿瘤细胞毒性与LPS诱导白细胞介素1(IL-1)分泌的能力或含有干扰素-γ的伴刀豆球蛋白A(Con A)上清液增加H-2和Ia表达的能力之间没有明显的相关性。因此,根据后一个标准,一个不能杀死肿瘤细胞的杂交瘤克隆仍然对LPS和淋巴因子激活敏感。