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- W4313351768 startingPage "125.1" @default.
- W4313351768 abstract "Abstract Asthma is a chronic inflammatory disease of the lungs marked by mast cell activation, eosinophilia, and airway remodeling. It has been seen that primary sensitization to inhaled allergens leads to increased production of allergen specific IgE and IgG1. Several studies have shown a critical role for IgE in allergic lung disease, but it is unclear how IgG1 might contribute to the initiation and perpetuation of this disease. Previous work in our lab identified a key role for FcγRIII on dendritic cells (DC) in the development of optimal Th2-dependent airway inflammation. As FcγRIII is efficiently engaged by IgG1-immune complexes, we hypothesized that sensitized individuals could form allergen-specific immune complexes upon secondary exposure which could contribute to the augmented Th2 responses found in allergic asthma. We used two different models of immune complex mediated Th2 inflammation through either immune complex formation in vivo or local installation of preformed immune complexes. Both models showed that this process was mediated through FcγRIII. Utilizing both in vitro and in vivo approaches, we then identified IL-33 as a gene downstream of FcγRIII signaling on DCs. Notably, immune complex mediated Th2 inflammation in the lungs was decreased in ST2-/- mice with a specific loss of eosinophilia suggesting a critical role for IL-33. Our findings that previous sensitization can direct the response of DCs could provide a new paradigm for the development of Th2 inflammation." @default.
- W4313351768 created "2023-01-06" @default.
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- W4313351768 date "2012-05-01" @default.
- W4313351768 modified "2023-09-30" @default.
- W4313351768 title "Allergen specific IgG augments Th2 mediated inflammation in the lungs through FcγRIII signaling and upregulation of IL-33 (125.1)" @default.
- W4313351768 doi "https://doi.org/10.4049/jimmunol.188.supp.125.1" @default.
- W4313351768 hasPublicationYear "2012" @default.
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