Interleukin-4 activates ion channels in B lymphocytes.

The lymphokine interleukin-4 (IL-4) has been shown to induce dramatic changes in the physiology of resting B cells. We have applied the patch clamp technique in the cell attached and inside/out configurations to resting and IL-4-treated B cells to determine whether specific ion conductances result as a consequence of IL-4 action. We report here that two distinct ion channel events occur in B lymphocytes after treatment with IL-4, (i) induction of an inward rectifying K+ channel that is not observed in untreated cells, and (ii) activation of a large conductance anion channel that is normally silent in non-treated cells in the cell attached patch configuration. These data present the first evidence of a direct effect by IL-4 on ion channels and we suggest roles for these two ionic conductances in IL-4-induced B cell activation.     

The growth factor IL-2 activates p21ras proteins in normal human T lymphocytes.

The T cell growth factor IL-2 induces T cell progression through the cell cycle and ultimately controls T cell mitosis. Here we show that the guanine nucleotide-binding proteins p21ras may be involved in IL-2 signal transduction pathways. IL-2 causes a rapid and prolonged activation of p21ras in both murine and human T cells. The concentration-dependence of IL-2-mediated stimulation of p21ras correlated with IL-2 stimulation of T cell proliferation, which indicates that p21ras activity can be controlled by signals generated via the interaction between IL-2 and its high affinity cellular receptor. These results suggest that p21ras may play a role in the regulation of T cell growth by IL-2.