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Allergin-1 Immunoreceptor Suppresses House Dust Mite–Induced Allergic Airway Inflammation
Author(s) -
Haruka Miki,
Satoko TaharaHanaoka,
Mariana Silva Almeida,
Kaori Hitomi,
Shohei Shibagaki,
Kazumasa Kanemaru,
Yu-Hsien Lin,
Kanako Iwata,
Shota Miyake,
Shiro Shibayama,
Takayuki Sumida,
Kazuko Shibuya,
Akira Shibuya
Publication year - 2020
Publication title -
the journal of immunology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.1900180
Subject(s) - immunology , house dust mite , allergic inflammation , immunoreceptor tyrosine based activation motif , integrin alpha m , cd11c , inflammation , syk , medicine , allergy , biology , immune system , t cell , allergen , tyrosine kinase , signal transduction , phenotype , microbiology and biotechnology , biochemistry , t cell receptor , gene
House dust mite (HDM) allergens are leading causes of allergic asthma characterized by Th2 responses. The lung-resident CD11b + dendritic cells (DCs) play a key role in Th2 cell development in HDM-induced allergic asthma. However, the regulatory mechanism of HDM-induced CD11b + DC activation remains incompletely understood. In this study, we demonstrate that mice deficient in an inhibitory immunoreceptor, Allergin-1, showed exacerbated HDM-induced airway eosinophilia and serum IgE elevation. By using bone marrow-chimeric mice that were sensitized with adoptively transferred HDM-stimulated wild-type or Allergin-1-deficient CD11b + bone marrow-derived cultured DCs (BMDCs), followed by challenge with HDM, we show that Allergin-1 on the BMDCs suppressed HDM-induced allergic airway inflammation. We also show that Allergin-1 suppressed HDM-induced PGE 2 production from CD11b + BMDCs by inhibiting Syk tyrosine kinase activation through recruitment of SHP-1, subsequently leading to negative regulation of Th2 responses. These results suggest that Allergin-1 plays an important role in regulation of HDM-induced allergic airway inflammation.

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