Chouaib S, Blay J Y
Laboratoire d'Immunologie, Institut Gustave-Roussy, Ville-Juie, France.
Pathol Biol (Paris). 1990 Jan;38(1):47-52.
The effect of Tumor Necrosis Factor (TNF) alpha on LAK generation was investigated. TNF was found to act synergistically with low concentrations of IL-2 (15 pM), which were ineffective by themselves to promote the differentiation of Large granular lymphocytes (LGL) into LAK effectors. The IL-2/TNF driven generation of LAK activity involves the induction of high affinity IL-2 receptors on LGL and occurs without promoting a significant proliferation, suggesting a functional activation rather than a proliferative expansion of LAK precursors. Our studies also indicate the existence of a correlation between the generation of LAK activity and the increase in TNF binding sites on LGL. Furthermore we demonstrate that the failure of low doses of IL-2 to induce LAK activity were related to their incapacity to induce TNF production by LGL and suggest that TNF alpha may be a physiologic mediator in the sequential activation stages of LGL into LAK effectors.
研究了肿瘤坏死因子（TNF）α对淋巴因子激活的杀伤细胞（LAK）生成的影响。发现TNF与低浓度的白细胞介素-2（IL-2，15皮摩尔）协同作用，低浓度的IL-2单独作用时不能促进大颗粒淋巴细胞（LGL）分化为LAK效应细胞。IL-2/TNF驱动的LAK活性生成涉及LGL上高亲和力IL-2受体的诱导，且在不促进显著增殖的情况下发生，这表明是LAK前体细胞的功能激活而非增殖性扩增。我们的研究还表明，LAK活性的生成与LGL上TNF结合位点的增加之间存在相关性。此外，我们证明低剂量IL-2不能诱导LAK活性与它们不能诱导LGL产生TNF有关，并提示TNFα可能是LGL依次激活为LAK效应细胞阶段的生理介质。
