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Spontaneous atopic dermatitis in mice with a defective skin barrier is independent of ILC 2 and mediated by IL ‐1β
Allergy ( IF 12.6 ) Pub Date : 2019-04-29 , DOI: 10.1111/all.13801 Christian Schwartz 1, 2 , Tara Moran 1, 3 , Sean P Saunders 1, 3 , Agnieszka Kaszlikowska 1, 3 , Achilleas Floudas 1, 3 , Joana Bom 4 , Gabriel Nunez 5 , Yoichiro Iwakura 6 , Luke O'Neill 7 , Alan D Irvine 3, 8 , Andrew N J McKenzie 9 , Graham Ogg 10 , Patrick T Walsh 3, 11 , Jocelyne Demengeot 4 , Padraic G Fallon 1, 3, 11
Allergy ( IF 12.6 ) Pub Date : 2019-04-29 , DOI: 10.1111/all.13801 Christian Schwartz 1, 2 , Tara Moran 1, 3 , Sean P Saunders 1, 3 , Agnieszka Kaszlikowska 1, 3 , Achilleas Floudas 1, 3 , Joana Bom 4 , Gabriel Nunez 5 , Yoichiro Iwakura 6 , Luke O'Neill 7 , Alan D Irvine 3, 8 , Andrew N J McKenzie 9 , Graham Ogg 10 , Patrick T Walsh 3, 11 , Jocelyne Demengeot 4 , Padraic G Fallon 1, 3, 11
Affiliation
Atopic dermatitis (AD) is one of the most common skin diseases with a multifactorial etiology. Mutations leading to loss of skin barrier function are associated with the development of AD with group 2 innate lymphoid cells (ILC2) promoting acute skin inflammation. Filaggrin‐mutant (Flgft/ft) mice develop spontaneous skin inflammation accompanied by an increase in skin ILC2 numbers, IL‐1β production, and other cytokines recapitulating human AD. Here, we investigated the role of ILC2, effector cytokines, inflammasome activation, and mast cell function on the development of chronic AD‐like inflammation in mice.
中文翻译:
皮肤屏障缺陷小鼠的自发性特应性皮炎不依赖于 ILC 2,由 IL ‐1β 介导
特应性皮炎(AD)是最常见的皮肤病之一,其病因有多种。导致皮肤屏障功能丧失的突变与 AD 的发展有关,其中第 2 类先天淋巴细胞 (ILC2) 会促进急性皮肤炎症。丝聚蛋白突变体 (Flgft/ft) 小鼠会出现自发性皮肤炎症,并伴有皮肤 ILC2 数量、IL-1β 产生和其他细胞因子的增加,这些细胞因子与人类 AD 相似。在这里,我们研究了 ILC2、效应细胞因子、炎症小体激活和肥大细胞功能在小鼠慢性 AD 样炎症发展中的作用。
更新日期:2019-04-29
中文翻译:
皮肤屏障缺陷小鼠的自发性特应性皮炎不依赖于 ILC 2,由 IL ‐1β 介导
特应性皮炎(AD)是最常见的皮肤病之一,其病因有多种。导致皮肤屏障功能丧失的突变与 AD 的发展有关,其中第 2 类先天淋巴细胞 (ILC2) 会促进急性皮肤炎症。丝聚蛋白突变体 (Flgft/ft) 小鼠会出现自发性皮肤炎症,并伴有皮肤 ILC2 数量、IL-1β 产生和其他细胞因子的增加,这些细胞因子与人类 AD 相似。在这里,我们研究了 ILC2、效应细胞因子、炎症小体激活和肥大细胞功能在小鼠慢性 AD 样炎症发展中的作用。