Sakamoto K M, Mignacca R C, Gasson J C
Department of Pediatrics, UCLA School of Medicine 90024-1752.
Recept Channels. 1994;2(3):175-81.
Granulocyte-macrophage colony stimulating factor (GM-CSF) and Interleukin-3 (IL-3) are cytokines which stimulate myeloid bone marrow progenitor cell proliferation and maturation. GM-CSF also enhances the function of terminally differentiated effector cells including neutrophils, monocytes and eosinophils. Both growth factors exhibit similar biological activities on overlapping cell populations which are mediated by high affinity receptors. These receptors share a common beta subunit necessary for signal transduction. The receptors for GM-CSF and IL-3 are members of the hematopoietin receptor superfamily and consequently lack intrinsic tyrosine kinase activity. Several kinases, including JAK2 and raf-1, and other downstream molecules are likely to be responsible for the functional redundancy demonstrated by GM-CSF and IL-3 in factor-responsive cells. This review discusses recent findings which elucidate the signaling pathways activated by these two cytokines.
粒细胞巨噬细胞集落刺激因子（GM-CSF）和白细胞介素-3（IL-3）是刺激骨髓祖细胞增殖和成熟的细胞因子。GM-CSF还可增强终末分化效应细胞的功能，包括中性粒细胞、单核细胞和嗜酸性粒细胞。这两种生长因子对重叠细胞群体表现出相似的生物学活性，这些活性由高亲和力受体介导。这些受体共享信号转导所必需的共同β亚基。GM-CSF和IL-3的受体是造血受体超家族的成员，因此缺乏内在的酪氨酸激酶活性。包括JAK2和raf-1在内的几种激酶以及其他下游分子可能是GM-CSF和IL-3在因子反应性细胞中表现出功能冗余的原因。本综述讨论了阐明这两种细胞因子激活的信号通路的最新研究结果。
