先天性淋巴细胞
先天免疫系统
免疫学
免疫系统
生物
白细胞介素22
细胞因子
白细胞介素
作者
Julie Deckers,Filipe Branco Madeira,Hamida Hammad
标识
DOI:10.1016/j.it.2013.08.004
摘要
•Innate cells contribute to the development of asthma features. •Epithelial cell–DC crosstalk is crucial for asthma development. •Epithelium-derived cytokines contribute to ILC2 responses. •Basophils have no role in Th2 sensitization to HDM, but contribute to the effector phase. Asthma is an inflammatory disease of the airways associated with a T helper (Th)2 response. Such a response in the lungs requires complex interactions between innate cells and structural cells. Dendritic cells (DCs) are pivotal during sensitization to allergens but clearly require epithelium-derived signals to become activated. Epithelial cells also contribute to the activation and the survival of mast cells (MCs), basophils, and eosinophils and group 2 innate lymphoid cells (ILC2s). In turn, these innate cells can activate DCs to sustain Th2 immunity. Here, we review the role played by these different populations of immune cells in the pathogenesis of asthma and how they interact to orchestrate Th2 immunity. Asthma is an inflammatory disease of the airways associated with a T helper (Th)2 response. Such a response in the lungs requires complex interactions between innate cells and structural cells. Dendritic cells (DCs) are pivotal during sensitization to allergens but clearly require epithelium-derived signals to become activated. Epithelial cells also contribute to the activation and the survival of mast cells (MCs), basophils, and eosinophils and group 2 innate lymphoid cells (ILC2s). In turn, these innate cells can activate DCs to sustain Th2 immunity. Here, we review the role played by these different populations of immune cells in the pathogenesis of asthma and how they interact to orchestrate Th2 immunity.
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