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肿瘤坏死因子α多态性与紫外线B光对皮肤免疫的有害影响相关。

Tumor necrosis factor alpha polymorphism correlates with deleterious effects of ultraviolet B light on cutaneous immunity.

作者信息

Vincek V, Kurimoto I, Medema J P, Prieto E, Streilein J W

机构信息

Department of Microbiology and Immunology, University of Miami School of Medicine, Florida 33136.

出版信息

Cancer Res. 1993 Feb 15;53(4):728-32.

PMID:8094030
Abstract

Intradermally injected tumor necrosis factor alpha (TNF-alpha) mimics the effects of UV B light (UVB) radiation and neutralizing anti-TNF-alpha antibodies abolish the deleterious effects of UVB on induction of contact hypersensitivity suggesting that TNF-alpha is the major mediator of UVB effects on cutaneous immunity. In the present study we have shown that in lipopolysaccharide-sensitive inbred strains of mice, the ability of acute, low-dose UVB radiation to impair the induction of contact hypersensitivity to dinitrofluorobenzene is genetically determined by polymorphic alleles at the Tnf alpha locus. We have analyzed by the sequence analysis and restriction fragment length polymorphism the Tnf alpha alleles of numerous inbred strains expressing UVB susceptibility (UVB-S) and UVB-resistance (UVB-R). The Tnf alpha alleles of all UVB-R, but not UVB-S, strains contain a BamHI site in the first intron. Moreover, the 5' regulatory region of the Tnf alpha allele of UVB-R mice possesses a (CA)14 minirepeat that is located immediately 5' of the cytokine response element nearest the tumor-associated transplantation antigen box. By contrast, the Tnf alpha alleles of UVB-S mice display repeats of < > 14 at this site. It is proposed that the unique microsatellite of UVB-R mice impairs transcriptional efficiency at Tnf alpha compared to UVB-S mice and that the quantitative difference in Tnf alpha produced intracutaneously in response to UVB radiation accounts for the phenotypic traits of UVB-R and UVB-S.

摘要

皮内注射肿瘤坏死因子α(TNF-α)可模拟紫外线B(UVB)辐射的作用,而中和性抗TNF-α抗体可消除UVB对诱导接触性超敏反应的有害影响,这表明TNF-α是UVB对皮肤免疫作用的主要介质。在本研究中,我们发现,在对脂多糖敏感的近交系小鼠中,急性低剂量UVB辐射损害对二硝基氟苯接触性超敏反应诱导的能力由Tnfα基因座的多态性等位基因遗传决定。我们通过序列分析和限制性片段长度多态性分析了众多表达UVB易感性(UVB-S)和UVB抗性(UVB-R)的近交系的Tnfα等位基因。所有UVB-R品系而非UVB-S品系的Tnfα等位基因在第一个内含子中含有一个BamHI位点。此外,UVB-R小鼠Tnfα等位基因的5'调控区具有一个(CA)14微重复序列,该序列位于最靠近肿瘤相关移植抗原盒的细胞因子反应元件的5'端紧邻处。相比之下,UVB-S小鼠的Tnfα等位基因在该位点的重复序列< > 14。有人提出,与UVB-S小鼠相比,UVB-R小鼠独特的微卫星损害了Tnfα的转录效率,并且对UVB辐射皮内产生的Tnfα的定量差异解释了UVB-R和UVB-S的表型特征。

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