Leonard R J, Garcia M L, Slaughter R S, Reuben J P
Department of Membrane Biochemistry and Biophysics, Merck Research Laboratories, Rahway, NJ 07065.
Proc Natl Acad Sci U S A. 1992 Nov 1;89(21):10094-8. doi: 10.1073/pnas.89.21.10094.
Charybdotoxin (ChTX), a K+ channel blocker, depolarizes human peripheral T lymphocytes and renders them insensitive to activation by mitogen. We observed four types of K+ channels in human T cells: one voltage-activated, and three Ca(2+)-activated. To discern the mechanism by which ChTX depolarizes T cells, we examined the sensitivity of both the voltage-activated and Ca(2+)-activated K+ channels to ChTX and other peptide channel blockers. All four types were blocked by ChTX, whereas noxiustoxin and margatoxin blocked only the voltage-activated channels. All three toxins, however, produced equivalent depolarization in human T cells. We conclude that the membrane potential of resting T cells is set by voltage-activated channels and that blockade of these channels is sufficient to depolarize resting human T cells and prevent activation.
蝎毒素（ChTX）是一种钾离子通道阻滞剂，可使人类外周血T淋巴细胞去极化，并使其对有丝分裂原激活不敏感。我们在人类T细胞中观察到四种类型的钾离子通道：一种是电压激活型，三种是钙激活型。为了探究ChTX使T细胞去极化的机制，我们检测了电压激活型和钙激活型钾离子通道对ChTX和其他肽类通道阻滞剂的敏感性。所有四种类型的通道都被ChTX阻断，而蜂毒明肽和边缘毒素仅阻断电压激活型通道。然而，这三种毒素在人类T细胞中产生的去极化作用相当。我们得出结论，静息T细胞的膜电位由电压激活型通道设定，阻断这些通道足以使静息的人类T细胞去极化并阻止其激活。
