Ravid A, Rubin A L, Novogrodsky A, Stenzel K H
Exp Cell Res. 1983 May;145(2):239-44. doi: 10.1016/0014-4827(83)90002-2.
ConA at high concentrations inhibits lymphocyte mitogenesis. Previous studies have shown that inhibitory conA concentrations do not inhibit the acquisition of responsiveness to interleukin-2 (IL-2) when excessive conA is removed. To analyse further the problem of high-dose inhibition by conA, we determined whether inhibition of mitogenesis is related to inhibition of IL-2 production or, alternatively, whether factor production is intact, but the cells are rendered incapable of responding to the factor. ConA stimulates IL2 production at concentrations that are inhibitory to mitogenesis of human lymphocytes. IL-2 was assayed both in a murine cytotoxic T cell line and human memory cells. The response of IL-2-dependent cells to Il-2-containing medium was, on the other hand, inhibited by conA in a dose-dependent fashion. One mechanism whereby high conA concentrations inhibit mitogenesis is by rendering cells resistant to IL-2, possibly via extensive cross-linking of cell surface sites.
高浓度的刀豆蛋白A（ConA）会抑制淋巴细胞的有丝分裂。先前的研究表明，当去除过量的ConA时，抑制性ConA浓度不会抑制对白介素-2（IL-2）反应性的获得。为了进一步分析ConA高剂量抑制的问题，我们确定有丝分裂的抑制是否与IL-2产生的抑制有关，或者相反，因子产生是否完整，但细胞变得无法对该因子作出反应。ConA在抑制人淋巴细胞有丝分裂的浓度下刺激IL-2的产生。在鼠细胞毒性T细胞系和人记忆细胞中都检测了IL-2。另一方面，ConA以剂量依赖性方式抑制IL-2依赖性细胞对含IL-2培养基的反应。高浓度ConA抑制有丝分裂的一种机制是使细胞对IL-2产生抗性，可能是通过细胞表面位点的广泛交联。
