Merritt W D, Bailey J M, Pluznik D H
Cell Immunol. 1984 Nov;89(1):1-10. doi: 10.1016/0008-8749(84)90191-6.
Previous work has shown that exogenous gangliosides suppress lectin-induced T-lymphocyte mitogenesis in mixed populations of immune cells. As one potential cellular site of this inhibition, the influence of gangliosides on interleukin-2-dependent T-cell proliferation was tested, using cultures of cytotoxic T cells (strain CT-6). Incubation of CT-6 cells with mixed bovine brain gangliosides resulted in a dose-dependent inhibition of cell proliferation. Cell viability was unaffected by gangliosides, and the inhibition was totally reversed when the gangliosides were removed. Individual purified gangliosides were tested and GM2 was most inhibitory (I50 = 15 microM). GD1a and GT1b were somewhat less potent, whereas GM1 and GM3 were only weakly inhibitory. Various nonpolar lipids, sulfatides, and sialic acid did not inhibit CT-6 cell growth. The results suggest that a primary mechanism whereby gangliosides inhibit lectin-induced lymphocyte mitogenesis is by inhibition of the interleukin-2-stimulated proliferation of T cells in these cultures.
先前的研究表明，外源性神经节苷脂可抑制免疫细胞混合群体中凝集素诱导的T淋巴细胞有丝分裂。作为这种抑制作用的一个潜在细胞位点，使用细胞毒性T细胞（CT-6株）培养物测试了神经节苷脂对白细胞介素-2依赖性T细胞增殖的影响。用混合牛脑神经节苷脂孵育CT-6细胞导致细胞增殖呈剂量依赖性抑制。神经节苷脂不影响细胞活力，去除神经节苷脂后抑制作用完全逆转。测试了单个纯化的神经节苷脂，GM2的抑制作用最强（半数抑制浓度I50 = 15 microM）。GD1a和GT1b的效力稍弱，而GM1和GM3仅具有微弱的抑制作用。各种非极性脂质、硫脂和唾液酸不抑制CT-6细胞生长。结果表明，神经节苷脂抑制凝集素诱导的淋巴细胞有丝分裂的主要机制是抑制这些培养物中白细胞介素-2刺激的T细胞增殖。
