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논문 기본 정보

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Pollaris Lore (Centre for Environment and Health Department of Public Health and Primary Care University of Leuven) Decaesteker Tatjana (Laboratory of Respiratory Diseases and Thoracic Surgery Department of Chronic Diseases and Metaboli) Van den Broucke Sofie (Centre for Environment and Health Department of Public Health and Primary Care University of Leuven) Jonckheere Anne-Charlotte (Department of Microbiology Immunology and Transplantation Allergy and Clinical Immunology Research) Cremer Jonathan (Department of Microbiology Immunology and Transplantation Allergy and Clinical Immunology Research) Verbeken Erik (Department of Imaging and Pathology University of Leuven Leuven Belgium.) Maes Tania (Laboratory for Translational Research in Obstructive Pulmonary Diseases Department of Respiratory M) Devos Fien C (Centre for Environment and Health Department of Public Health and Primary Care University of Leuven) Vande Velde Greetje (Department of Imaging and Pathology Biomedical MRI University of Leuven Leuven Belgium.) Nemery Benoit (Centre for Environment and Health Department of Public Health and Primary Care University of Leuven) Hoet Peter H. M. (Centre for Environment and Health Department of Public Health and Primary Care University of Leuven) Vanoirbeek Jeroen A. J. (Centre for Environment and Health Department of Public Health and Primary Care University of Leuven)
저널정보
대한천식알레르기학회(구 대한알레르기학회) Allergy, Asthma & Immunology Research Allergy, Asthma & Immunology Research Vol.13 No.2
발행연도
2021.1
수록면
295 - 311 (17page)

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Purpose: Exposure to low concentrations of toluene diisocyanate (TDI) leads to immune-mediated chemical-induced asthma. The role of the adaptive immune system has already been thoroughly investigated; nevertheless, the involvement of innate immune cells in the pathophysiology of chemical-induced asthma is still unresolved. The aim of the study is to investigate the role of innate lymphoid cells (ILCs) and dendritic cells (DCs) in a mouse model for chemical-induced asthma. Methods: On days 1 and 8, BALB/c mice were dermally treated (20 μL/ear) with 0.5% TDI or the vehicle acetone olive oil (AOO; 2:3). On days 15, 17, 19, 22 and 24, the mice received an oropharyngeal challenge with 0.01% TDI or AOO (1:4). One day after the last challenge, airway hyperreactivity (AHR) to methacholine was assessed, followed by an evaluation of pulmonary inflammation and immune-related parameters, including the cytokine pattern in bronchoalveolar lavage fluid, lymphocyte subpopulations of the lymph nodes and their ex vivo cytokine production profile, blood immunoglobulins and DC and ILC subpopulations in the lungs. Results: Both DC and ILC2 were recruited to the lungs after multiple airway exposures to TDI, regardless of the prior dermal sensitization. However, prior dermal sensitization with TDI alone results in AHR and predominant eosinophilic airway inflammation, accompanied by a typical type 2 helper T (Th2) cytokine profile. Conclusions: TDI-induced asthma is mediated by a predominant type 2 immune response, with the involvement of adaptive Th2 cells. However, from our study we suggest that the innate ILC2 cells are important additional players in the development of TDI-induced asthma.

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