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Dectin-1 Plays an Important Role in House Dust Mite-Induced Allergic Airway Inflammation through the Activation of CD11b+ Dendritic Cells.
- Source :
-
Journal of Immunology . 1/1/2017, Vol. 198 Issue 1, p61-70. 10p. - Publication Year :
- 2017
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Abstract
- It is well known that sensitization against fungi is closely associated with severity of asthma. Dectin-1 (gene symbol Clec7a), a C-type lectin receptor, recognizes the fungal cell wall component b-glucan, as well as some component(s) in house dust mite (HDM) extract. However, the roles of Dectin-1 in HDM-induced allergic airway inflammation remain unclear. In this study, we used Dectin-1-deficient (Clec7a-/-) mice to examine whether Dectin-1 is involved in HDM-induced allergic airway inflammation. We found that HDM-induced eosinophil and neutrophil recruitment into the airways was significantly attenuated in Clec7a-/- mice compared with that in wild-type mice. In addition, HDM-induced IL-5, IL-13, and IL-17 production from mediastinum lymph node cells was reduced in HDM-sensitized Clec7a-/- mice. Dectin-1 was expressed on CD11b+ dendritic cells (DCs), an essential DC subset for the development of allergic inflammation, but not on CD103+ DCs, plasmacytoid DCs, or lung epithelial cells. Transcriptome analysis revealed that the expression of chemokine/chemokine receptors, including CCR7, which is indispensable for DC migration to draining lymph nodes, was decreased in Clec7a-/- DCs. In accordance with these results, the number of HDM-labeled CD11b+ DCs in mediastinum lymph nodes was significantly reduced in Clec7a-/- mice compared with wild-type mice. Taken together, these results suggest that Dectin-1 expressed on CD11b+ DCs senses some molecule(s) in HDM extract and plays a critical role in the induction of HDM-induced allergic airway inflammation by inducing the expression of chemokine/chemokine receptors in DCs. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00221767
- Volume :
- 198
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Journal of Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 120389810
- Full Text :
- https://doi.org/10.4049/jimmunol.1502393