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抗炎药物对树突状细胞细胞因子产生的差异性抑制作用

Differential suppression of dendritic cell cytokine production by anti-inflammatory drugs.

作者信息

Toebak M J, de Rooij J, Moed H, Stoof T J, von Blomberg B M E, Bruynzeel D P, Scheper R J, Gibbs S, Rustemeyer T

机构信息

Department of Dermatology, VU University Medical Centre, Amsterdam, The Netherlands.

出版信息

Br J Dermatol. 2008 Feb;158(2):225-33. doi: 10.1111/j.1365-2133.2007.08297.x. Epub 2007 Nov 19.

DOI:10.1111/j.1365-2133.2007.08297.x
PMID:18028503
Abstract

BACKGROUND

Various anti-inflammatory drugs are available for the treatment of skin disorders. In these diseases, untoward immune responses to endogenous and/or environmental antigens are initiated by maturation and polarization of dendritic cells (DC).

OBJECTIVE

To explore the suppressive effects of anti-inflammatory drugs on DC maturation and, in particular, polarization.

METHODS

Exposure of DC to nickel in vitro results in DC maturation and secretion of both type 1 and type 2 cytokines, thereby providing a model to study the effects of anti-inflammatory drugs on DC responses. The inhibitory effects of anti-inflammatory drugs (ciclosporin, dexamethasone, diclofenac, dimethylfumarate, hydrocortisone, lactoferrin, 1-alpha,25-dihydroxyvitamin D3) on DC maturation (CD83, CD86, HLA-DR, CXCL8) and polarization (type 1: IL-12p70, TNF-alpha; type 2: IL-10, CCL17) were studied.

RESULTS

All anti-inflammatory drugs, except for lactoferrin, had inhibitory effects on DC maturation. Hydrocortisone and dexamethasone exclusively suppressed the release of type 1 cytokines. A less pronounced, but similar profile was observed for dimethylfumarate and 1-alpha,25-dihydroxyvitamin D3. Ciclosporin suppressed both type 1 and 2 cytokines. In contrast, diclofenac suppressed only type 2 DC cytokine secretion.

CONCLUSION

The present results give more insight into the pharmacological effects of immunosuppressive drugs on the immune system, and can thereby contribute to a more rational selection of anti-inflammatory drugs for the treatment of inflammatory skin disorders.

摘要

背景

有多种抗炎药物可用于治疗皮肤疾病。在这些疾病中，树突状细胞（DC）的成熟和极化引发了对内源性和/或环境抗原的不良免疫反应。

目的

探讨抗炎药物对DC成熟尤其是极化的抑制作用。

方法

在体外将DC暴露于镍会导致DC成熟并分泌1型和2型细胞因子，从而提供一个研究抗炎药物对DC反应影响的模型。研究了抗炎药物（环孢素、地塞米松、双氯芬酸、富马酸二甲酯、氢化可的松、乳铁蛋白、1-α,25-二羟基维生素D3）对DC成熟（CD83、CD86、HLA-DR、CXCL8）和极化（1型：IL-12p70、TNF-α；2型：IL-10、CCL17）的抑制作用。

结果

除乳铁蛋白外，所有抗炎药物均对DC成熟有抑制作用。氢化可的松和地塞米松仅抑制1型细胞因子的释放。富马酸二甲酯和1-α,25-二羟基维生素D3观察到的抑制作用较不明显但相似。环孢素抑制1型和2型细胞因子。相比之下，双氯芬酸仅抑制2型DC细胞因子的分泌。

结论

本研究结果更深入地揭示了免疫抑制药物对免疫系统的药理作用，从而有助于更合理地选择抗炎药物来治疗炎症性皮肤病。

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