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巨噬细胞诱导CD163依赖性血红蛋白摄取作为糖皮质激素的一种新型抗炎作用。

Induction of the CD163-dependent haemoglobin uptake by macrophages as a novel anti-inflammatory action of glucocorticoids.

作者信息

Schaer Dominik J, Boretti Felicitas S, Schoedon Gabriele, Schaffner Andreas

机构信息

Medizinische Klinik B, Department of Internal Medicine, University Hospital of Zurich, Switzerland.

出版信息

Br J Haematol. 2002 Oct;119(1):239-43. doi: 10.1046/j.1365-2141.2002.03790.x.

DOI:10.1046/j.1365-2141.2002.03790.x
PMID:12358930
Abstract

Highly efficient systems remove toxic and pro-inflammatory haemoglobin (Hb) from the circulation and local sites of tissue damage. Macrophages are major Hb-clearing cells; CD163 was recently recognized as the specific haemoglobin-haptoglobin scavenger receptor (HSR). We show that dexamethasone strongly induced the specific uptake of haemoglobin-haptoglobin complexes, CD163 mRNA transcription (13-fold) and cell surface expression (10-fold) by human macrophages. In contrast, the TH2-cytokine interleukin 4 (IL-4) completely suppressed functional CD163 expression. The range of functional receptor modulation reached a factor of 100 after 4 h of macrophage-ligand interaction. Based on these results, we propose the augmentation of Hb clearance as a novel anti-inflammatory action of glucocorticoids.

摘要

高效系统可从循环系统和组织损伤局部部位清除有毒和促炎血红蛋白(Hb)。巨噬细胞是主要的Hb清除细胞;CD163最近被确认为特异性血红蛋白-结合珠蛋白清除受体(HSR)。我们发现,地塞米松可强烈诱导人巨噬细胞特异性摄取血红蛋白-结合珠蛋白复合物、CD163 mRNA转录(13倍)和细胞表面表达(10倍)。相比之下,TH2细胞因子白细胞介素4(IL-4)可完全抑制功能性CD163的表达。巨噬细胞与配体相互作用4小时后,功能性受体调节范围达到100倍。基于这些结果,我们提出增强Hb清除作为糖皮质激素一种新的抗炎作用。

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