Auf1/Hnrnpd-deficient mice develop pruritic inflammatory skin disease.
Auf1/Hnrnpd-deficient mice develop pruritic inflammatory skin disease.
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DOI：
10.1038/jid.2008.298
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发表时间：
2009-03
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影响因子：
--
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中科院分区：
文献类型：
--
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缺乏异源核核糖核蛋白D（Hnrnpd）（也称为Auf 1，一种炎症细胞因子mRNA稳定性的调节剂）的小鼠会随着年龄的增长而发生慢性皮炎，其特征在于皮炎和表皮脱落。组织学分析显示明显的表皮棘层和海绵状组织增生、新生血管形成和炎性细胞数量增加，包括T细胞、巨噬细胞、中性粒细胞、肥大细胞和嗜酸性粒细胞。患有皮炎的Hnrnpdtm 1 Rjsc缺陷型小鼠显示血清IgE水平升高。Hnrnpdtm 1 Rjsc小鼠中的病变与向Th 2免疫环境的转变相关。通过测定接触性超敏反应评价T细胞介导的皮肤炎症，表明Hnrnpdtm 1 Rjsc小鼠的反应增加。来自Hnrnpdtm 1 Rjsc小鼠的T细胞和巨噬细胞表现出许多与皮炎相关的异常，包括IL 2、肿瘤坏死因子-α（TNFα）和IL 1 β产生增加。最后，在未受影响的Hnrnpdtm 1 Rjsc小鼠中，通过皮下注射CCL 27和TNF，可以在实验诱导的病变中重现自发性皮炎的许多特征。总的来说，这些数据突出了HNRNPD和mRNA稳定性的适当调节在皮肤内白细胞募集和炎症活化的复杂过程中的重要性。
Mice lacking heterogenous nuclear ribonuclear protein D (Hnrnpd), also known as Auf1, a regulator of inflammatory cytokine mRNA stability, develop chronic dermatitis with age that is characterized by pruritis and excoriations. Histological analysis showed marked epidermal acanthosis and spongiosis, neovascularization, and elevated number of inflammatory cells, including T cells, macrophages, neutrophils, mast cells, and eosinophils. Hnrnpd-deficient (Hnrnpdtm1Rjsc) mice with dermatitis display elevated serum IgE levels. Lesions in Hnrnpdtm1Rjsc mice were associated with a shift towards a Th2 immune environment. Evaluation of T-cell-mediated skin inflammation by assaying contact hypersensitivity indicated an increased response in Hnrnpdtm1Rjsc mice. T cells and macrophages from Hnrnpdtm1Rjsc mice demonstrate a number of abnormalities associated with dermatitis, including increased IL2, tumor-necrosis factor-α (TNFα), and IL1β production. Finally, many features of spontaneous dermatitis could be recapitulated in experimentally induced lesions by subcutaneous injection of CCL27 and TNF in unaffected Hnrnpdtm1Rjsc mice. Collectively, these data highlight the importance of HNRNPD and proper regulation of mRNA stability in the intricate processes of leukocyte recruitment and inflammatory activation within the skin.
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影响因子：
14.2
作者：
de Vries, IJM;Langeveld-Wildschut, EG;Bruijnzeel-Koomen, CAFM
通讯作者：
Bruijnzeel-Koomen, CAFM
影响因子：
4.1
作者：
Hon, KLE;Leung, TF;Fok, TF
通讯作者：
Fok, TF
影响因子：
14.9
作者：
Barreau C;Paillard L;Osborne HB
通讯作者：
Osborne HB
影响因子：
14.9
作者：
Bhattacharya, S;Giordano, T;Malter, JS
通讯作者：
Malter, JS
影响因子：
6.5
作者：
Nagelkerken, Lex;Verzaal, Perry;Oranje, Arnold P.
通讯作者：
Oranje, Arnold P.