Kusunoki T, Tsuruta S, Higashi H, Hosoi S, Hata D, Sugie K, Mayumi M, Mikawa H
Division of Pediatrics, South Kyoto National Hospital, Japan.
J Leukoc Biol. 1994 Jun;55(6):735-42. doi: 10.1002/jlb.55.6.735.
Neutrophils showed a rapid and transient adhesion to immunoglobulin G (IgG)-coated plates compared with their adhesion to bovine serum albumin (BSA)-coated plates: the adhesion reached a peak after 15 min of incubation and then gradually returned to almost the basal state in 60 min. The addition of monomeric IgG or anti-Fc gamma RII monoclonal antibody (mAb) (IV.3) suppressed the increase in adhesion, whereas anti-Fc gamma RIII mAb (3G8) was hardly effective, indicating that the interaction of Fc gamma R, especially Fc gamma RII, with coated IgG is involved in the process. Adhesion was also blocked by cytochalasin B, suggesting that functional actin filament structures are crucial. Protein kinase inhibitors, erbstatin and genistein, inhibited the adhesion in a dose-dependent manner. The adhesion was inhibited by anti-CD11b (M1/70) and anti-CD18 (MHM23, TS1/18) mAbs. Moreover, neutrophils from a patient with complete leukocyte adhesion deficiency syndrome did not show increased adhesion to IgG-coated plates. The adhesion of neutrophils to fibrinogen- and BSA-coated plates was also increased when Fc gamma R was stimulated in the fluid phase with soluble aggregated IgG, which was also inhibited by anti-CD11b mAb. Stimulation of neutrophil Fc gamma R with soluble aggregated IgG enhanced the expression of CD11b in concert with the enhanced adhesion. These data collectively suggest that stimulation via Fc gamma R evokes a tyrosine kinase-dependent and actin filament-dependent intracellular signal that enhances the specific and nonspecific adhesive activity of neutrophils, presumably through the activation of CD11b/CD18.
与嗜中性粒细胞对牛血清白蛋白（BSA）包被平板的黏附相比，它们对免疫球蛋白G（IgG）包被平板表现出快速且短暂的黏附：孵育15分钟后黏附达到峰值，然后在60分钟内逐渐恢复到几乎基础状态。添加单体IgG或抗FcγRII单克隆抗体（mAb）（IV.3）可抑制黏附增加，而抗FcγRIII mAb（3G8）几乎无效，表明FcγR，尤其是FcγRII与包被的IgG之间的相互作用参与了该过程。细胞松弛素B也可阻断黏附，提示功能性肌动蛋白丝结构至关重要。蛋白激酶抑制剂埃博霉素和染料木黄酮以剂量依赖方式抑制黏附。抗CD11b（M1/70）和抗CD18（MHM23，TS1/18）mAb可抑制黏附。此外，来自完全白细胞黏附缺陷综合征患者的嗜中性粒细胞对IgG包被平板未表现出黏附增加。当用可溶性聚集IgG在液相中刺激FcγR时，嗜中性粒细胞对纤维蛋白原和BSA包被平板的黏附也会增加，抗CD11b mAb也可抑制这种增加。用可溶性聚集IgG刺激嗜中性粒细胞FcγR会增强CD11b的表达，并伴随着黏附增强。这些数据共同表明，通过FcγR的刺激引发了酪氨酸激酶依赖性和肌动蛋白丝依赖性的细胞内信号，该信号增强了嗜中性粒细胞的特异性和非特异性黏附活性，可能是通过激活CD11b/CD18实现的。
