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1α,25 - 二羟维生素D3和细胞因子对人单核吞噬细胞上IgA、IgE和IgG Fc受体表达的调节作用

Modulation of IgA, IgE, and IgG Fc receptor expression on human mononuclear phagocytes by 1 alpha,25-dihydroxyvitamin D3 and cytokines.

作者信息

Boltz-Nitulescu G, Willheim M, Spittler A, Leutmezer F, Tempfer C, Winkler S

机构信息

Institute of General and Experimental Pathology, University of Vienna, Austria.

出版信息

J Leukoc Biol. 1995 Aug;58(2):256-62. doi: 10.1002/jlb.58.2.256.

Abstract

The effects of 1 alpha,25-dihydroxyvitamin D3/calcitriol on the expression of Fc receptors (FcR) for IgA (Fc alpha R), IgE (Fc epsilon RII), and IgG (Fc gamma R) on human peripheral blood monocytes and the cell lines U937, THP-1, and Mono Mac-6, in combination with various cytokines, was examined by flow cytometry. On both monocyte-derived macrophages and the myelomonocytic cell lines, Fc alpha R/CD89 expression was induced by calcitriol alone and additively in combination with tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), and granulocyte-macrophage colony-stimulating factor. Constitutive and interleukin-4 (IL-4)-driven Fc epsilon RII/CD23 expression was markedly diminished on calcitriol-treated U937 cells and monocytes. Fc epsilon RII was also triggered by IFN-gamma, TNF-alpha, and IL-6 on all the cell lines, an effect blocked by calcitriol. On monocytes, the basal level and IFN-gamma-induced Fc gamma RI/CD64 expression was down-regulated by calcitriol and IL-4. The expression of Fc gamma RII/CD32 on monocytes was strongly suppressed by calcitriol. Transforming growth factor-beta induced Fc gamma RIII/CD16 on monocytes, an effect opposed by calcitriol. The ability of calcitriol-treated monocytes to phagocytose IgG-sensitized ox erythrocytes was diminished. Our results demonstrate that calcitriol, alone or in combination with cytokines, modulates Fc alpha R, Fc epsilon RII, Fc gamma RI, and Fc gamma RII expression on human mononuclear phagocytes, as well as Fc gamma R-mediated phagocytosis.

摘要

采用流式细胞术检测了1α,25 - 二羟基维生素D3/骨化三醇对人外周血单核细胞以及细胞系U937、THP - 1和Mono Mac - 6上IgA(FcαR)、IgE(FcεRII)和IgG(FcγR)的Fc受体(FcR)表达的影响,同时检测了其与多种细胞因子联合作用的情况。在单核细胞衍生的巨噬细胞和骨髓单核细胞系上,骨化三醇单独即可诱导FcαR/CD89表达,与肿瘤坏死因子-α(TNF-α)、干扰素-γ(IFN-γ)和粒细胞-巨噬细胞集落刺激因子联合使用时具有累加效应。在经骨化三醇处理的U937细胞和单核细胞上,组成性和白细胞介素-4(IL-4)驱动的FcεRII/CD23表达明显降低。在所有细胞系上,IFN-γ、TNF-α和IL-6也可触发FcεRII表达,而这一效应被骨化三醇阻断。在单核细胞上,骨化三醇和IL-4可下调基础水平以及IFN-γ诱导的FcγRI/CD64表达。骨化三醇可强烈抑制单核细胞上FcγRII/CD32的表达。转化生长因子-β可诱导单核细胞上FcγRIII/CD16表达,而骨化三醇则起相反作用。经骨化三醇处理的单核细胞吞噬IgG致敏的氧化红细胞的能力降低。我们的结果表明,骨化三醇单独或与细胞因子联合使用时,可调节人单核吞噬细胞上FcαR、FcεRII、FcγRI和FcγRII的表达,以及FcγR介导的吞噬作用。

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