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IL-33-dependent induction of allergic lung inflammation by FcγRIII signaling.
Tjota, Melissa Y; Williams, Jesse W; Lu, Tiffany; Clay, Bryan S; Byrd, Tiara; Hrusch, Cara L; Decker, Donna C; de Araujo, Claudia Alves; Bryce, Paul J; Sperling, Anne I.
Afiliación
  • Tjota MY; Committee on Immunology, University of Chicago, Chicago, Illinois 60637, USA.
J Clin Invest ; 123(5): 2287-97, 2013 May.
Article en En | MEDLINE | ID: mdl-23585480
Atopic asthma is a chronic inflammatory disease of the lungs generally marked by excessive Th2 inflammation. The role of allergen-specific IgG in asthma is still controversial; however, a receptor of IgG-immune complexes (IgG-ICs), FcγRIII, has been shown to promote Th2 responses through an unknown mechanism. Herein, we demonstrate that allergen-specific IgG-ICs, formed upon reexposure to allergen, promoted Th2 responses in two different models of IC-mediated inflammation that were independent of a preformed T cell memory response. Development of Th2-type airway inflammation was shown to be both FcγRIII and TLR4 dependent, and T cells were necessary and sufficient for this process to occur, even in the absence of type 2 innate lymphoid cells. We sought to identify downstream targets of FcγRIII signaling that could contribute to this process and demonstrated that bone marrow-derived DCs, alveolar macrophages, and respiratory DCs significantly upregulated IL-33 when activated through FcγRIII and TLR4. Importantly, IC-induced Th2 inflammation was dependent on the ST2/IL-33 pathway. Our results suggest that allergen-specific IgG can enhance secondary responses by ligating FcγRIII on antigen-presenting cells to augment development of Th2-mediated responses in the lungs via an IL-33-dependent mechanism.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Interleucinas / Receptores de IgG / Inflamación / Pulmón Límite: Animals Idioma: En Revista: J Clin Invest Año: 2013 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Interleucinas / Receptores de IgG / Inflamación / Pulmón Límite: Animals Idioma: En Revista: J Clin Invest Año: 2013 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos