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Scientific memory from the early nineties; a common project with professors late János Gergely and Anna Erdei
Biologia Futura ( IF 1.8 ) Pub Date : 2021-01-10 , DOI: 10.1007/s42977-020-00056-y
Andras Falus 1 , Zsuzsa Bajtay 2
Affiliation  

Based on the findings of common project 29 years ago, the Scandinavian J. of Immunology accepted and published our paper entitled by “FcγR-Dependent Regulation of the Biosynthesis of Complement C3 by Murine Macrophages: the Modulatory Effect of IL-6” (Bajtay et al. in SJI 35:195–201, 1992). In this report we attempt to review the previous results and evaluate them with our current concepts on the interaction between the actors of adaptive and innate immunity. Let us first to summarize the basic results and consequences from the paper from 1992. Abstract from 1991–1992: The effect of murine IgG isotypes (myeloma proteins) on the gene expression and secretion of the third component of complement (C3) has been studied using the in monocytoid cell line P388D1 and oil-elicited mouse peritoneal macrophages. It is demonstrated that the binding of lgG2a and lgG2b but not IgGl and IgG3 isotypes augments the biosynthesis of C3 both in the presence and in the absence of the phorbol myristate acetate in the case of both cell types. The multifunctional cytokine inlerleukin-6 (IL-6) alone reveals no effect on the gene expression of C3, but facilitates the effectiveness of mouse IgG2a and IgG2b. Confirming the role of FcgRll, a strong up-regulation of gene expression and secretion of C3 was found when macrophages were co-cultured with the F(ab')2 fragment of the FcγRII-specific monoclonal antibody 2.4 G2.



中文翻译:

九十年代初的科学记忆;与已故教授 János Gergely 和 Anna Erdei 的共同项目

基于29年前共同项目的研究结果,斯堪的纳维亚免疫学杂志接受并发表了我们的论文,题为“FcγR-Dependent Regulation of the Biosynthesis of Complement C3 by Murine Macrophages: the Modulatory Effect of IL-6”(Bajtay et al. 在 SJI 35:195-201, 1992)。在本报告中,我们试图回顾以前的结果,并用我们当前关于适应性和先天免疫参与者之间相互作用的概念对其进行评估。让我们首先总结一下 1992 年论文的基本结果和后果。 1991-1992 年摘要:研究了小鼠 IgG 同种型(骨髓瘤蛋白)对补体第三种成分 (C3) 的基因表达和分泌的影响使用单核细胞系 P388D1 和油诱导的小鼠腹膜巨噬细胞。证明在两种细胞类型的情况下,在存在和不存在佛波醇肉豆蔻酸酯乙酸酯的情况下,IgG2a和IgG2b而非IgG1和IgG3同种型的结合增强了C3的生物合成。单独的多功能细胞因子 inlerleukin-6 (IL-6) 对 C3 的基因表达没有影响,但促进了小鼠 IgG2a 和 IgG2b 的有效性。证实 FcgRll 的作用,当巨噬细胞与 FcγRII 特异性单克隆抗体 2.4 G2 的 F(ab')2 片段共培养时,发现基因表达和 C3 分泌的强烈上调。单独的多功能细胞因子 inlerleukin-6 (IL-6) 对 C3 的基因表达没有影响,但促进了小鼠 IgG2a 和 IgG2b 的有效性。证实 FcgRll 的作用,当巨噬细胞与 FcγRII 特异性单克隆抗体 2.4 G2 的 F(ab')2 片段共培养时,发现基因表达和 C3 分泌的强烈上调。单独的多功能细胞因子 inlerleukin-6 (IL-6) 对 C3 的基因表达没有影响,但促进了小鼠 IgG2a 和 IgG2b 的有效性。证实 FcgRll 的作用,当巨噬细胞与 FcγRII 特异性单克隆抗体 2.4 G2 的 F(ab')2 片段共培养时,发现基因表达和 C3 分泌的强烈上调。

更新日期:2021-01-10
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