Type I IL-4Rs selectively activate IRS-2 to induce target gene expression in macrophages.

摘要: Although interleukin-4 (IL-4) and IL-13 participate in allergic inflammation share a receptor subunit (IL-4Rα), they have different functions. We compared cells expressing type I II IL-4Rs with only receptors for their responsiveness to these cytokines. IL-4 induced highly efficient, γC-dependent tyrosine phosphorylation of insulin substrate 2 (IRS-2), whereas was less effective, even when signal transducer activator transcription 6 (STAT6) maximal. Only receptor, signaling efficient association IRS-2 the p85 phosphoinositide 3-kinase or adaptor protein growth factor receptor–bound 2. In addition, through more robust expression subset genes associated alternatively activated macrophages than did IL-13. Thus, activates pathways qualitatively differently from IL-13, which cooperate induce optimal gene expression.