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Selective blockers and manipulated channel expression levels

Summary To maintain Ca 2+ entry during T lymphocyte activation, a balancing efflux of cations is necessary. Using three approaches, we demonstrate that this cation efflux is mediated by Ca 2+ -activated K + (K Ca ) channels, h SKCa2 in the human leukemic T cell line Jurkat and h IKCa1 in mitogen-activated human T cells. First, several recently developed, selective and potent pharmacological inhibitors of K Ca channels but not K V channels reduce Ca 2+ entry in Jurkat and in mitogen-activated human T cells. Second, dominant-negative suppression of the native K Ca channel in Jurkat T cells by over-expression of a truncated fragment of the cloned hSKCa2 channel decreases Ca 2+ influx. Finally, introduction of the h IKCa1 channel into Jurkat T cells maintains rapid Ca 2+ entry despite pharmacological inhibition of the native small-conductance K Ca channel. Thus K Ca channels play a vital role in T cell Ca 2+ signaling. INTRODUCTION The human leukemic T cell line, Jurkat, is widely used as a model system to study intracellular signaling cascades during lymphocyte activation. These studies have revealed the critical requirement for two signaling pathways to complete lymphocyte activation. In the first pathway, activation of protein kinase-C (PKC)