A NOVEL, NH2-TERMINAL SEQUENCE CHARACTERIZED HUMAN MONOKINE POSSESSING NEUTROPHIL CHEMOTACTIC, SKIN-REACTIVE, AND GRANULOCYTOSIS-PROMOTING ACTIVITY
A NOVEL, NH2-TERMINAL SEQUENCE CHARACTERIZED HUMAN MONOKINE POSSESSING NEUTROPHIL CHEMOTACTIC, SKIN-REACTIVE, AND GRANULOCYTOSIS-PROMOTING ACTIVITY
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DOI：
10.1084/jem.167.4.1364
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发表时间：
1988-04-01
影响因子：
15.3
通讯作者：
BILLIAU, A
中科院分区：
文献类型：
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作者：
VANDAMME, J;VANBEEUMEN, J;BILLIAU, A
在有丝分裂原刺激的人血白细胞上清液中检测到一种能够诱导兔皮肤早期局部炎症的因子。该因子与IL-1不同，IL-1虽然存在于上清液中，但可与该因子化学分离，并诱导晚期而非早期皮肤反应。主因子的其他生物学效应是其对粒细胞的体外趋化作用和其在兔静脉注射后诱导快速粒细胞增多的能力。当在相同条件下测试时，IL-1 β不起趋化作用，并在稍后的时间诱导粒细胞增多症。将该因子纯化至均一，并通过电泳迁移率鉴定为Mr 6，500的蛋白质。氨基酸序列分析显示存在未受污染的NH 2-末端序列，该序列与先前从cDNA克隆（3- 10 C）中预测的序列片段相同，该cDNA克隆从人白细胞分离的mRNA中复制，并编码未知功能的蛋白质。该因子的NH 2-末端序列也显示出与血小板因子β-血小板球蛋白（β TG）和血小板因子4（PF-4）的广泛同源性。鉴定该因子的细胞来源的研究表明，它是由粘附的单核细胞产生的，而不是由血小板产生的，而β TG则相反。
A factor able to induce an early local inflammation in rabbit skin was detected in the supernatant of mitogen-stimulated human blood leukocytes. The factor was different from IL-1 which, although present in the supernatants, was chemically separable from the factor and induced a late rather than an early skin response. Other biological effects of the principal factor were its in vitro chemotactic effects on granulocytes and its ability to induce rapid granulocytosis upon intravenous injection in rabbits. When tested under the same conditions, IL-1 beta did not act chemotactically and induced granulocytosis at a later time. The factor was purified to homogeneity and identified by electrophoretic mobility as a protein of Mr 6,500. Amino acid sequence analysis revealed the presence of an uncontaminated NH2-terminal sequence identical to a segment of the sequence previously predicted from the cDNA clone (3-10C) copied from an mRNA isolated from human leukocytes and coding for a protein of unknown function. The NH2-terminal sequence of the factor also showed extensive homology to that of the platelet factors beta-thromboglobulin (beta TG) and platelet factor 4 (PF-4). Studies done to identify the cell source of the factor revealed that it was produced by adherent mononuclear cells but not by platelets, while the opposite was true for beta TG.