Cytokine production and function in c-mpl-deficient mice:: No physiologic role for interleukin-3 in residual megakaryocyte and platelet production
Cytokine production and function in c-mpl-deficient mice:: No physiologic role for interleukin-3 in residual megakaryocyte and platelet production
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DOI：
10.1182/blood.v91.8.2745.2745_2745_2752
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发表时间：
1998-04-15
期刊：
影响因子：
20.3
通讯作者：
Alexander, WS
中科院分区：
文献类型：
--
作者：
Gainsford, T;Roberts, AW;Alexander, WS
缺乏血小板生成素（TPO）或其受体c-Mpl的小鼠，表现出巨核细胞和血小板发育缺陷以及多种造血谱系祖细胞缺陷。在mpl（-/-）小鼠中检查了在TPO信号传导不存在的情况下替代细胞因子对血小板生成的贡献。血清和器官条件培养基的分析表明，没有证据表明巨核细胞生成细胞因子的代偿性过度生产。然而，与体内的潜在作用一致，当注射到mpl（-/-）小鼠中时，白细胞介素-6（IL-6）和白血病抑制因子（LIF）保留了在造血组织中升高巨核细胞及其祖细胞并增加循环血小板数量的能力。然而，培育为携带c-Mpl和IL-3或IL-3受体α链的遗传缺陷的双突变小鼠，与缺乏mpl的动物相比，没有显示出更大的巨核细胞或血小板缺陷，这表明在这些小鼠中，IL-3在残余的巨核细胞生成和血小板产生中不起生理作用。(C)1998年，美国血液学会。
Mice lacking thrombopoietin (TPO), or its receptor c-Mpl, display defective megakaryocyte and platelet development and deficiencies in progenitor cells of multiple hematopoietic lineages. The contribution of alternative cytokines to thrombopoiesis in the absence of TPO signalling was examined in mpl(-/-) mice. Analysis of serum and organ-conditioned media showed no evidence of a compensatory overproduction of megakaryocytopoietic cytokines. However, consistent with a potential role in vivo, when injected into mpl(-/-) mice, interleukin-6 (IL-6) and leukemia inhibitory factor (LIF) retained the capacity to elevate megakaryocytes and their progenitors in hematopoietic tissues and increase circulating platelet numbers, However, double mutant mice bred to carry genetic defects both in c-Mpl and IL-3 or the alpha chain of the IL-3 receptor, displayed no greater deficiencies in megakaryocytes or platelets than mpl-deficient animals, suggesting absence of a physiologic role for IL-3 in the residual megakaryocytopoiesis and platelet production in these mice. (C) 1998 by The American Society of Hematology.