BONE-MARROW ABNORMALITIES IN THE NONOBESE DIABETIC MOUSE
BONE-MARROW ABNORMALITIES IN THE NONOBESE DIABETIC MOUSE
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DOI：
10.1093/intimm/5.2.169
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发表时间：
1993-02-01
影响因子：
4.4
通讯作者：
CRISPE, IN
中科院分区：
文献类型：
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作者：
LANGMUIR, PB;BRIDGETT, MM;CRISPE, IN
一些证据表明非肥胖糖尿病（NOD）小鼠骨髓谱系细胞的表型、细胞因子反应和功能异常。在这项研究中，我们的特点是表型和髓系祖细胞功能的NOD骨髓。两种造血分化抗原Ly-6C和AA4.1在NOD骨髓细胞上异常表达。虽然多系红骨髓祖细胞（第12天CFU-S）在NOD小鼠中的数量是正常的，但更分化的髓系祖细胞在体外对IL-3、粒细胞/巨噬细胞集落刺激因子（GM-CSF）和IL-5的应答是缺陷的。由于NOD小鼠易患糖尿病的Idd-5基因与IL-1受体关系密切，我们检测了NOD小鼠骨髓细胞中IL-1和IL-3协同作用的缺陷，没有发现缺陷。
Several lines of evidence point to abnormalities of the phenotype, cytokine responses, and function of cells of the myeloid lineage in non-obese diabetic (NOD) mice. In this study we have characterized the phenotype and myeloid progenitor function of NOD bone marrow. Two hematopoietic differentiation antigens, Ly-6C and AA4.1, are expressed abnormally on NOD bone marrow cells. While multilineage erythromyeloid progenitor cells (day 12 CFU-S) are normal in number in NOD mice, more differentiated myeloid progenitors are deficient in their in vitro responses to IL-3, granulocyte/macrophage colony-stimulating factor (GM-CSF), and IL-5. Since the diabetes-predisposing Idd-5 gene of NOD mice maps close to the IL-1 receptor, we tested NOD bone marrow cells for a defect in synergy between IL-1 and IL-3; no defect was found. The defects in myelopoiesis described here may predispose the NOD mouse to autoimmunity by impairing macrophage maturation.