A monoclonal antibody to the membrane glycoprotein complex CD18 inhibits polymorphonuclear leukocyte accumulation and plasma leakage in vivo.

A monoclonal antibody to the membrane glycoprotein complex CD18 inhibits polymorphonuclear leukocyte accumulation and plasma leakage in vivo.
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DOI:
10.1182/blood.v69.1.338.338
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发表时间:
1987
期刊:
影响因子:
20.3
通讯作者:
K. Arfors;C. Lundberg;L. Lindbom;K. Lundberg;P. Beatty;J. Harlan
K. Arfors;C. Lundberg;L. Lindbom;K. Lundberg;P. Beatty;J. Harlan
中科院分区:
医学1区
文献类型:
--
作者:
K. Arfors;C. Lundberg;L. Lindbom;K. Lundberg;P. Beatty;J. Harlan

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先前的体外研究结果表明,多形核白细胞 (PMN) 膜糖蛋白复合物 CD18 在 PMN 粘附和趋化性中发挥着关键作用。我们检测了识别 CD18 的鼠单克隆抗体 (MoAb) 60.3 对诱导体内 PMN 积累的影响。家兔用MoAb 60.3预处理,皮内注射趋化因子fMLP、白三烯(LT)B4和C5a以及组胺; 4小时后,测定血浆渗漏(125I-白蛋白)和PMN积累(髓过氧化物酶)。与对照动物相比,用 MoAb 60.3 预处理的兔子的炎症性皮损中 PMN 积累和 PMN 依赖性血浆渗漏均被消除,而组胺诱导的 PMN 无关血浆渗漏不受影响。兔细小肌的活体显微镜检查显示,在应用 LTB4 和酵母聚糖激活血清 (ZAS) 后,MoAb 60.3 抑制 PMN 在小静脉中的粘附和迁移到组织中。 PMN 沿小静脉内皮的滚动不受影响。因此,这些实验证实并扩展了早期的体外发现,即膜糖蛋白复合物 CD18 在 PMN 粘附和趋化性中的关键作用。
Previous in vitro findings suggest a critical role for the polymorphonuclear leukocyte (PMN) membrane glycoprotein complex CD18 in PMN adherence and chemotaxis. We examined the effect of the murine monoclonal antibody (MoAb) 60.3, recognizing CD18, on induced PMN accumulation in vivo. Rabbits were pretreated with MoAb 60.3, and the chemotactic factors fMLP, leukotriene (LT)B4, and C5a, as well as histamine, were injected intradermally; 4 hours later, plasma leakage (125I-albumin) and the PMN accumulation (myeloperoxidase) were determined. Both PMN accumulation and PMN-dependent plasma leakage were abolished in the inflammatory skin lesions of rabbits pretreated with MoAb 60.3 as compared with control animals, whereas histamine-induced PMN-independent plasma leakage was unaffected. Intravital microscopy of the rabbit tenuissimus muscle revealed that MoAb 60.3 inhibited both PMN adherence in the venules and migration into the tissue following application of LTB4 and zymosan-activated serum (ZAS). Rolling of PMNs along the venular endothelium was unaffected. Thus, these experiments confirm and extend earlier in vitro findings of the critical role of the membrane glycoprotein complex, CD18, in PMN adherence and chemotaxis.