Suppression of PAMPs, Pathogen-Associated Microbial Patterns, Induced Cytokine Synthesis of PBMC, Human Blood Mononuclear Cells, by Immunoglobulin Preparation

A. Yamamoto, N. Miura, T. Oharaseki, Kei Takahashi, S. Naoe, Kazuo Suzuki, N. Ohno
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Abstract

The applications of immunoglobulin preparation for intravenous injection (IVIg) for various intractable dis- eases are increasing. The two major clinical indications for IVIg are the replacement therapy and the anti-inflammation therapy for a variety of acute and chronic autoimmune diseases. One of the proposed mechanisms of IVIg activity is the modulation of cytokine expression and function; therefore, we analyzed the effect of IVIg on pathogen-associated mo- lecular pattern (PAMP)-induced cytokine production by peripheral blood mononuclear cells (PBMCs). The production of tumor necrosis factor- (TNF- ) as a result of stimulation with lipopolysaccharide (LPS), polyinosinic-polycytidylic acid sodium salt (Poly I:C), or Pam3CysSerLys4 (Pam3) was significantly inhibited by sulfonated-IVIg (S-IVIg), or by F(ab')2. Assessed by one-color microarray analysis, the expressions of 229 genes were inhibited to 1/200 or less by F(ab')2. On the other hand, the expressions of 159 genes were increased by more than 100-fold by F(ab')2. According to these results, it was suggested that IVIg inhibits inflammatory PAMPs-induced cytokine production by PBMCs, due to the modulation of varieties of gene expression.
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免疫球蛋白制剂抑制PAMPs,病原体相关微生物模式,诱导PBMC,人血单核细胞的细胞因子合成
静脉注射用免疫球蛋白制剂(IVIg)在各种顽固性疾病中的应用越来越广泛。IVIg的两大临床适应症是各种急慢性自身免疫性疾病的替代治疗和抗炎治疗。IVIg活性的机制之一是细胞因子表达和功能的调节;因此,我们分析了IVIg对病原体相关分子模式(PAMP)诱导外周血单个核细胞(PBMCs)产生细胞因子的影响。由脂多糖(LPS)、聚肌苷-多胞酸钠盐(Poly I:C)或Pam3CysSerLys4 (Pam3)刺激产生的肿瘤坏死因子(TNF-)被磺化- ivig (S-IVIg)或F(ab')2显著抑制。单色微阵列分析显示,F(ab’)2对229个基因表达抑制至1/200以下。另一方面,F(ab’)2使159个基因的表达量增加了100倍以上。根据这些结果,我们认为IVIg抑制炎症pamps诱导的PBMCs产生细胞因子可能是通过调节基因表达的多样性来实现的。
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