calcium, which performs a wide variety of functions within the cell, has very important roles as a immune response mediator. This study examined effects of the calcium/calmodulin system on suppression of human NK cell function by glucocorticoid.
Verapamil, a calcium channel blocker, and pimozide, a calmodulin antagonist, further increased the suppression of NK cell activity inhibited by dexamethasone. Addition of CaCl2 resulted in significant mitigation of the suppresion of NK cell
function by
dexamethasone and verapamil or pimozide combined. BAY K8644 and calcium ionohore. A23187, also were shown to faciitate some attenuastion of inhibition of NK cell function by dexamethasone. With the assumption that expression of mRNA for cytokines
reflects activity of the NK cel, dexamethasone and verapamil were shown to suppress NK cell function(lower expression of mRNA for cytokine, IFN-γ). Atthe other end, BAY K86447 and CaCl2 showed a recovery of suppressed NK cell function by
dexamethasone
as evidenced by an increased expression of mRNA for IFN-γcompared to expressions shown for dexamethasone alone. thus, it could be well deduced that suppression of the influx in the cell of calcium and of the calcium-calmodulin system may be an
important mechanism for suppresion of NK cell function by glucocorticoids.
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