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豚鼠多形核白细胞上两种不同的Fcγ受体在引发超氧阴离子生成的活性方面彼此不同。

Two distinct Fc gamma Rs on guinea-pig polymorphonuclear leukocytes differ from each other in their eliciting activities for O2- generation.

作者信息

Sato M, Nakamura T, Koyama J

机构信息

Department of Hygienic Chemistry, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.

出版信息

Mol Immunol. 1988 Feb;25(2):205-11. doi: 10.1016/0161-5890(88)90069-7.

Abstract

When guinea-pig polymorphonuclear leukocytes (PMNs) are stimulated with hen ovalbumin (OA)-complexed IgG antibodies, they generate superoxide anion (O2-). This reaction was found to depend on the IgG isotype used for preparation of the immune complexes; OA-complexed IgG2 antibody (OA-IgG2) induced 3-4 times more intensively O2- generation than OA-complexed IgG1 antibody (OA-IgG1). The O2- generation with OA-IgG1 was almost completely inhibited by a monoclonal antibody to the Fc gamma R binding both IgG1 and IgG2 (Fc gamma 1/gamma 2 R), whereas that with OA-IgG2 was only slightly inhibited. Since guinea-pig PMNs are capable of binding OA-IgG2 not only through Fc gamma 1/gamma 2 R but also through another Fc gamma R which is specific for IgG2 alone (Fc gamma 2 R), the O2- generation with OA-IgG2 may be mainly mediated by Fc gamma 2 R. In addition, cytochalasin B was found to enhance markedly the O2- generation with OA-IgG1, though that with OA-IgG2 was only slightly affected. The results so far obtained indicate that Fc gamma 1/gamma 2 R and Fc gamma 2 R differ from each other in their activities for triggering O2- generation, namely activation of the respiratory burst NADPH oxidase. Furthermore, differing from the activation of the NADPH oxidase mediated by Fc gamma 2 R, that by Fc gamma 1/gamma 2 R was shown to be suppressed by some cytochalasin B-inhibitable factor or process though its biochemical nature is unknown.

摘要

当用与鸡卵清蛋白(OA)复合的IgG抗体刺激豚鼠多形核白细胞(PMN)时,它们会产生超氧阴离子(O2-)。发现该反应取决于用于制备免疫复合物的IgG同种型;与OA复合的IgG2抗体(OA-IgG2)诱导产生O2-的强度比与OA复合的IgG1抗体(OA-IgG1)高3至4倍。用针对同时结合IgG1和IgG2的FcγR的单克隆抗体(Fcγ1/γ2R)几乎完全抑制了OA-IgG1诱导的O2-产生,而OA-IgG2诱导的O2-产生仅受到轻微抑制。由于豚鼠PMN不仅能够通过Fcγ1/γ2R结合OA-IgG2,还能通过另一种仅对IgG2特异的FcγR(Fcγ2R)结合,因此OA-IgG2诱导的O2-产生可能主要由Fcγ2R介导。此外,发现细胞松弛素B可显著增强OA-IgG1诱导的O2-产生,而对OA-IgG2诱导的O2-产生仅有轻微影响。迄今为止获得的结果表明,Fcγ1/γ2R和Fcγ2R在触发O2-产生的活性方面彼此不同,即呼吸爆发NADPH氧化酶的激活。此外,与Fcγ2R介导的NADPH氧化酶激活不同,Fcγ1/γ2R介导的激活被某种细胞松弛素B可抑制的因子或过程所抑制,尽管其生化性质尚不清楚。

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