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[Involvement of tumor necrosis factor in the generation of LAK killer cells]
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.
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.