San Marco M P, Pommier G J, Chabrol M C, Adda D H, Depieds R C
J Natl Cancer Inst. 1984 May;72(5):1101-11.
Cytosol fraction(s) from McFiFi2(s) fibrosarcoma cells (Fcc), isolated from either cultured cells or solid tumors induced in F344 rats, produced a dose-related inhibition of lymphoproliferative responses to several mitogens, whatever the lymphoid organ or the animal species used as the source of lymphocytes. Only stimulated human lymphocytes were not Fcc inhibited; instead, Fcc was a potent stimulator of their spontaneous proliferation. Fcc cytostatic activity was not effective in various cycling cell lines and was restricted to mitogen-stimulated lymphocytes. Fcc, a primary tumor product, did not induce suppressive cells and was unable to prevent mitogen cell surface binding. However, expression of its modulating effect was accelerated by the simultaneous presence of the mitogen. Moreover, Fcc produced its suppression by interrupting lymphocyte activation at some point within the G0-G1-phase transition. Molecular sieving showed that Fcc contains at least two factors with suppressive (mol wt, approximately 3,000) and stimulatory (mol wt, greater than 5,000) activities, respectively.
从F344大鼠中培养的细胞或实体瘤中分离出的McFiFi2纤维肉瘤细胞(Fcc)的胞质溶胶组分,对几种有丝分裂原诱导的淋巴细胞增殖反应产生剂量相关的抑制作用,无论用作淋巴细胞来源的淋巴器官或动物物种是什么。只有受刺激的人淋巴细胞不受Fcc抑制;相反,Fcc是其自发增殖的有效刺激物。Fcc的细胞生长抑制活性在各种循环细胞系中无效,并且仅限于有丝分裂原刺激的淋巴细胞。Fcc作为原发性肿瘤产物,不诱导抑制性细胞,也不能阻止有丝分裂原与细胞表面结合。然而,有丝分裂原的同时存在加速了其调节作用的表达。此外,Fcc通过在G0-G1期转变的某个点中断淋巴细胞活化来产生抑制作用。分子筛显示Fcc至少含有两种分别具有抑制活性(分子量约为3000)和刺激活性(分子量大于5000)的因子。