Biology of Lung Dendritic Cells at the Origin of Asthma
Dendritic cells (DCs) initiate and maintain adaptive T helper 2 (Th2) cell responses to inhaled allergens in asthma. Various functions like antigen uptake, migration to the draining LNs, and induction of tolerance and adaptive immunity are not equally shared by all subsets of DCs, adding considerable complexity to understanding the immunology of allergic sensitization. Whereas the epithelium was initially considered solely as a physical barrier, it is now seen as a central player in controlling the function of lung DCs through release of Th2 cell-promoting cytokines. Although DCs are sufficient and necessary for induction of Th2 cell responses to many antigens, some allergens might require antigen presentation by basophils. Clinically relevant allergens, as well as environmental and genetic risk factors for allergy and asthma, often interfere directly or indirectly with the innate immune functions of airway epithelial cells, basophils, and DCs. This review summarizes the recent progress on our understanding how DCs control Th2 cell immunity in the lung.
|Keywords||5 (6 carboxyhexyl) 1 (3 cyclohexyl 3 hydroxypropyl)hydantoin, Th2 cell, adaptive immunity, air pollution, allergen, antigen presentation, asthma, basophil, bwc 245c, cell function, cell migration, cell subpopulation, cellular immunity, cold air, cytokine production, cytology, dendritic cell, desensitization, disease exacerbation, environmental factor, exercise, fingolimod, heredity, human, immunological tolerance, innate immunity, interleukin 10, interleukin 13, interleukin 4, interleukin 5, lung alveolus cell, lymphatic drainage, nonhuman, pathogenesis, priority journal, respiratory epithelium, review, risk factor, rosiglitazone, sensitization, steroid, tumor necrosis factor, unclassified drug|
|Persistent URL||dx.doi.org/10.1016/j.immuni.2009.08.008, hdl.handle.net/1765/17408|
Lambrecht, B.N.M., & Hammad, H.. (2009). Biology of Lung Dendritic Cells at the Origin of Asthma. Immunity, 31(3), 412–424. doi:10.1016/j.immuni.2009.08.008