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本文引用的文献

1
Mast cells in photodamaged skin: what is their role in skin cancer?光损伤皮肤中的肥大细胞:它们在皮肤癌中起什么作用?
Photochem Photobiol Sci. 2006 Feb;5(2):177-83. doi: 10.1039/b504344a. Epub 2005 Sep 7.
2
Corticotropin-releasing hormone induces vascular endothelial growth factor release from human mast cells via the cAMP/protein kinase A/p38 mitogen-activated protein kinase pathway.促肾上腺皮质激素释放激素通过环磷酸腺苷/蛋白激酶A/p38丝裂原活化蛋白激酶途径诱导人肥大细胞释放血管内皮生长因子。
Mol Pharmacol. 2006 Mar;69(3):998-1006. doi: 10.1124/mol.105.019539. Epub 2005 Dec 6.
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DNA damage initiates photobiologic reactions in the skin.DNA损伤引发皮肤中的光生物学反应。
Photochem Photobiol Sci. 2005 Sep;4(9):709-14. doi: 10.1039/b417759m. Epub 2005 Jul 25.
4
Role of p38 MAPK in UVB-induced inflammatory responses in the skin of SKH-1 hairless mice.p38丝裂原活化蛋白激酶在UVB诱导的SKH-1无毛小鼠皮肤炎症反应中的作用
J Invest Dermatol. 2005 Jun;124(6):1318-25. doi: 10.1111/j.0022-202X.2005.23747.x.
5
Bivalent effect of UV light on human skin mast cells-low-level mediator release at baseline but potent suppression upon mast cell triggering.紫外线对人皮肤肥大细胞的双重作用——基线时低水平介质释放,但肥大细胞被触发时则产生强效抑制。
J Invest Dermatol. 2005 Feb;124(2):453-6. doi: 10.1111/j.0022-202X.2004.23523.x.
6
Biphasic expression of two paracrine melanogenic cytokines, stem cell factor and endothelin-1, in ultraviolet B-induced human melanogenesis.紫外线B诱导的人类黑素生成中两种旁分泌黑素生成细胞因子——干细胞因子和内皮素-1的双相表达
Am J Pathol. 2004 Dec;165(6):2099-109. doi: 10.1016/S0002-9440(10)63260-9.
7
Neutrophils infiltrating ultraviolet B-irradiated normal human skin display high IL-10 expression.浸润于紫外线B照射的正常人类皮肤中的中性粒细胞呈现出高白细胞介素-10表达。
Arch Dermatol Res. 2005 Jan;296(7):339-42. doi: 10.1007/s00403-004-0522-z. Epub 2004 Nov 18.
8
p38 Mitogen-Activated protein kinase mediates dual role of ultraviolet B radiation in induction of maturation and apoptosis of monocyte-derived dendritic cells.p38丝裂原活化蛋白激酶介导紫外线B辐射在诱导单核细胞衍生树突状细胞成熟和凋亡中的双重作用。
J Invest Dermatol. 2004 Aug;123(2):361-70. doi: 10.1111/j.0022-202X.2004.23238.x.
9
UVB-elicited induction of MMP-1 expression in human ocular surface epithelial cells is mediated through the ERK1/2 MAPK-dependent pathway.紫外线B(UVB)诱导人眼表上皮细胞中基质金属蛋白酶-1(MMP-1)表达是通过细胞外信号调节激酶1/2(ERK1/2)丝裂原活化蛋白激酶(MAPK)依赖途径介导的。
Invest Ophthalmol Vis Sci. 2003 Nov;44(11):4705-14. doi: 10.1167/iovs.03-0356.
10
Altered cutaneous immune parameters in transgenic mice overexpressing viral IL-10 in the epidermis.表皮中过表达病毒白细胞介素-10的转基因小鼠皮肤免疫参数的改变
J Clin Invest. 2003 Jun;111(12):1923-31. doi: 10.1172/JCI15722.

紫外线B照射可选择性增加人脐带血来源肥大细胞中白细胞介素-8的产生。

Ultraviolet B irradiation selectively increases the production of interleukin-8 in human cord blood-derived mast cells.

作者信息

Endoh I, Di Girolamo N, Hampartzoumian T, Cameron B, Geczy C L, Tedla N

机构信息

Centre for Inflammation and Infectious Diseases, School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia.

出版信息

Clin Exp Immunol. 2007 Apr;148(1):161-7. doi: 10.1111/j.1365-2249.2007.03332.x.

DOI:10.1111/j.1365-2249.2007.03332.x
PMID:17286758
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1868850/
Abstract

UVB irradiation modulates immune responses in the skin and is a major cause of sunburn, during which neutrophils accumulate in the skin. Because of their abundance in skin and ability to produce a variety of proinflammatory mediators, we propose that mast cells may play a key role in ultraviolet B (UVB)-induced skin inflammation. Cord blood-derived human mast cells were treated in vitro with varying doses of UVB and production of multiple cytokines was measured in culture supernatants. UVB exposure significantly increased the release of interleukin (IL)-8 and modestly increased IL-1alpha production, but cytokines such as IL-2, IL-4, IL-6, IL-10, IL-12, IL-13, tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma were unaffected. Cycloheximide reduced the UVB-mediated induction of IL-8 by 30-40%, suggesting that new protein synthesis contributed to IL-8 production. In line with this, UVB treatment of mast cells significantly increased IL-8 mRNA. In contrast to its effect on IL-8 production, optimal doses of UVB did not provoke histamine or tryptase release, indicating little effect on degranulation. Our data suggest that mast cells may play a major role during UVB-induced acute inflammation by selectively inducing cytokines involved in neutrophil recruitment.

摘要

紫外线B(UVB)照射可调节皮肤中的免疫反应,是晒伤的主要原因,在此过程中嗜中性粒细胞会在皮肤中积聚。由于肥大细胞在皮肤中数量众多且能够产生多种促炎介质,我们提出肥大细胞可能在紫外线B(UVB)诱导的皮肤炎症中起关键作用。用不同剂量的UVB对脐血来源的人肥大细胞进行体外处理,并测定培养上清液中多种细胞因子的产生情况。UVB照射显著增加了白细胞介素(IL)-8的释放,并适度增加了IL-1α的产生,但诸如IL-2、IL-4、IL-6、IL-10、IL-12、IL-13、肿瘤坏死因子(TNF)-α和干扰素(IFN)-γ等细胞因子未受影响。放线菌酮使UVB介导的IL-8诱导减少30-40%,这表明新的蛋白质合成有助于IL-8的产生。与此一致的是,UVB处理肥大细胞显著增加了IL-8 mRNA。与其对IL-8产生的影响相反,最佳剂量的UVB不会引发组胺或类胰蛋白酶的释放,表明对脱颗粒作用影响很小。我们的数据表明,肥大细胞可能通过选择性诱导参与嗜中性粒细胞募集的细胞因子,在UVB诱导的急性炎症中起主要作用。