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Interleukin 2 stimulates T cell proliferation using a calcium flux
A preparation enriched in rat interleukin 2 caused enhanced DNA synthesis in an interleukin 2-dependent mouse cytotoxic T cell line, in lectin transformed mouse splenocytes and in rat thymocytes. The enhanced proliferation due to interleukin 2 could be abrogated by chelating calcium from the culture medium or blocking calcium entry into the cells. Compounds which interfere with the function of calmodulin also inhibited proliferation. The addition of interleukin 2 to IL-2 dependent cells caused an increase in the intracellular concentration of calcium ions, as measured using Quin 2. The requirement for IL-2 by blasts and thymocytes could be replaced by calcium ionophore. The results implicate a calcium flux as an essential component of the action of interleukin 2 on its target cells.
A preparation enriched in rat interleukin 2 caused enhanced DNA synthesis in an interleukin 2-dependent mouse cytotoxic T cell line, in lectin transformed mouse splenocytes and in rat thymocytes. The enhanced proliferation due to interleukin 2 could be abrogated by chelating calcium from the culture medium or blocking calcium entry into the cells. Compounds which interfere with the function of calmodulin also inhibited proliferation. The addition of interleukin 2 to IL-2 dependent cells caused an increase in the intracellular concentration of calcium ions, as measured using Quin 2. The requirement for IL-2 by blasts and thymocytes could be replaced by calcium ionophore. The results implicate a calcium flux as an essential component of the action of interleukin 2 on its target cells.