Surface and intracellular interleukin-2 receptor expression on various resting and activated populations involved in cell-mediated immunity in human peripheral blood

Abstract

The kinetics of assembly of the high-affinity interleukin-2 receptor (IL-2R)α/β/γ were investigated by studying intracellular and surface expression of IL-2Rα,β and γ by T cells, monocytes and natural killer (NK) cells. IL-2Rα and IL-2Rγ were expressed by small numbers of resting T cells. These numbers increased following stimulation, to maximal expression at 48 h and 72 h, respectively. This observation was consistent with de novo synthesis of the receptor protein in response to the stimulus. The proportion of T cells producing IL-2Rβ was smaller and up-regulated later than the proportion of cells producing IL-2Rα or IL-2Rγ. IL-2Rβ may therefore slow the assembly of the high-affinity IL-2R on T cells. A small number of resting NK cells expressed IL-2Rα, both on the cell surface and intracellularly, but this increased over 72 h on stimulated NK cells. IL-2Rβ was constitutively expressed, both on the cell surface and intracellularly, by monocytes and NK cells. An increased proportion of NK cells and monocytes produced IL-2Rβ, 24 h and 4 h post-stimulation, respectively. Maximal or plateau expression occurred at 72 h and 24 h post-stimulation, for NK cells and monocytes, respectively. The early up-regulation of intracellular IL-2Rβ for monocytes may facilitate the upregulation of surface IL-2Rβ, and early assembly of the high-affinity IL-2R, accelerating monocyte activation and function. High constitutive intracellular IL-2Rγ expression (> 80%) in all types of leucocyte investigated, decreased over the 72 h following stimulation with a concurrent increase in surface expression. IL-2Rγ was expressed by increased proportions of T cells, monocytes and NK cells, 4 h following stimulation. The intracellular storage of IL-2Rγ may accelerate translocation to the cell surface after stimulation. The early translocation of IL-2Rγ may reflect its usage as a signal transduction molecule by other cytokine receptors - IL-4, IL-7, IL-9 and IL-15. This study delineated the potential expression of the high-affinity IL-2Rα/β/γ on various stimulated leucocytes. The differential kinetics of assembly of the high-affinity IL-2Rα/β/γ on different leucocyte subsets suggests that IL-2 may regulate the inflammatory cellular responses in a sequential manner, paralleling the timed expression of IL-2Rα/β/γ on the monocytes, NK cells and T cells.