Interleukin (1L)-2 activation of p2lraS in murine myeloid cells transfected with human IL-2 receptor p chain
The T cell growth factor interleukin-2 (IL-2) induces ~21'"' activation in T lymphocytes. To determine whether the IL-2 receptor (IL-2R) can regulate p2lraS when expressed in a non-Tcell environment we have examined the ability of IL-2 to activate p21ras in 32D murine myeloid progenitor cells transduced with human IL-2R fi chains. These cells are denoted 853 cells. 32D cells normally proliferate in response to IL-3 but the expression of the IL-2R fi chain confers IL-2 responsiveness to the cells. Our data show that IL-3 is able to activate p21ra5 in the parental 32D cells and both IL-2 and IL-3 can stimulate ~21'"' in the IL-2R-expressing 853 clone of 32D. I n T lymphocytes, activation of protein kinase C (PKC) with phorbol esters is sufficient to stimulate ~21'"'. However, in 32D and 853 cells activation of PKC with phorbol esters does not result in p21ras activation even though these cells express functional PKC. It appears, therefore, that a PKC-mediated pathway for ~21'"' regulation exists in T lymphocytes but not in 32D cells. The IL-2R can couple to p2lra' independently of the concomitant presence of the PKC pathway for p21ra5 regulation.These data imply that multiple intracellular mechanisms may exist to regulate ~21'"' and that cells of different lineages may differ with regard to p21raS regulation.