کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3356484 1217265 2006 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Death receptor-6 regulates the development of pulmonary eosinophilia and airway inflammation in a mouse model of asthma
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Death receptor-6 regulates the development of pulmonary eosinophilia and airway inflammation in a mouse model of asthma
چکیده انگلیسی

Death receptor-6 (DR6), a member of the death domain-containing TNFR superfamily, is highly expressed in lymphoid tissues and regulated upon lymphocyte activation. Targeted disruption of DR6 results in enhanced CD4+ T cell proliferation and T helper 2 (Th2) differentiation in vitro, whereas the in vivo role of DR6 in regulating Th2 cell differentiation and effector function remains largely unknown. In the current study, we used a Th2-skewed allergic airway inflammation model induced by ovalbumin (OVA) sensitization and challenge to compare the inflammatory response in the lung of both wild type (WT) and DR6−/− mice. DR6−/− mice were protected from the development of airway inflammation as evidenced by attenuated eosinophil accumulation and reduced mucus-producing cells in the lining airways of allergen-challenged animals. Consistent with these observations, a profound reduction of Th2 cytokine production (IL-5 and IL-13) was detected in the bronchoalveolar lavage fluid (BAL). Furthermore, a significant increase in the frequency of IFN-γ secreting cells was observed in the DR6−/− mouse lungs after OVA challenge, which may account for the reduced pulmonary Th2 cytokine production. These data point to a critical role of DR6 in regulating airway inflammation in the OVA-induced mouse model of asthma.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunology Letters - Volume 106, Issue 1, 15 July 2006, Pages 42–47
نویسندگان
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