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J Clin Invest ; 123(5): 2287-97, 2013 May.
Artigo em Inglês | MEDLINE | ID: mdl-23585480

RESUMO

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.


Assuntos
Inflamação/metabolismo , Interleucinas/metabolismo , Pulmão/patologia , Receptores de IgG/metabolismo , Animais , Asma/metabolismo , Células da Medula Óssea/citologia , Células Dendríticas/citologia , Ensaio de Imunoadsorção Enzimática , Feminino , Citometria de Fluxo , Hipersensibilidade , Hipersensibilidade Imediata/metabolismo , Imunoglobulina G/metabolismo , Interleucina-33 , Leucócitos Mononucleares/citologia , Macrófagos/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Transdução de Sinais , Células Th2
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