胸腺基质淋巴细胞生成素
免疫系统
细胞生物学
免疫学
生物
染色质
细胞因子
炎症
背景(考古学)
角质形成细胞
促炎细胞因子
基因
细胞培养
遗传学
古生物学
作者
Mariko Kashiwagi,Junichi Hosoi,Jen-Feng Lai,Janice L. Brissette,Steven F. Ziegler,Bruce Morgan,Katia Georgopoulos
摘要
Environmental challenges to epithelial cells trigger gene expression changes that elicit context-appropriate immune responses. We found that the chromatin remodeler Mi-2β controls epidermal homeostasis by regulating the genes involved in keratinocyte and immune-cell activation to maintain an inactive state. Mi-2β depletion resulted in rapid deployment of both a pro-inflammatory and an immunosuppressive response in the skin. A key target of Mi-2β in keratinocytes is the pro-inflammatory cytokine thymic stromal lymphopoietin (TSLP). Loss of TSLP receptor (TSLPR) signaling specifically in regulatory T (Treg) cells prevented their activation and permitted rapid progression from a skin pro-inflammatory response to a lethal systemic condition. Thus, in addition to their well-characterized role in pro-inflammatory responses, keratinocytes also directly support immune-suppressive responses that are critical for re-establishing organismal homeostasis.
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