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Trif-dependent induction of Th17 immunity by lung dendritic cells #MMPMID24985082
Mucosal Immunol 2015[Jan]; 8 (1): 186-97 PMID24985082show ga
Allergic asthma is thought to stem largely from maladaptive T helper (Th)2 responses to inhaled allergens, which in turn lead to airway eosinophilia and airway hyperresponsiveness. However, many individuals with asthma have airway inflammation that is predominantly neutrophilic and resistant to treatment with inhaled glucocorticoids. An improved understanding of the molecular basis of this form of asthma might lead to improved strategies for its treatment. Here, we identify novel roles of the adaptor protein, TRIF, in neutrophilic responses to inhaled allergens. In different mouse models of asthma, Trif-deficient animals had marked reductions in interleukin (IL)-17, airway neutrophils, and airway hyperresponsiveness compared with WT mice, whereas airway eosinophils were generally similar in these two strains. Compared with lung dendritic cells (DCs) from WT mice, lung DCs from Trif-deficient mice displayed impaired LPS-induced migration to regional lymph nodes, lower levels of the costimulatory molecule, CD40, and produced smaller amounts of the Th17-promoting cytokines, IL-6 and IL-1?. When cultured with allergen-specific, naïve T cells, Trif-deficient lung DCs stimulated robust Th2 cell differentiation, but very weak Th1 and Th17 cell differentiation. Together, these findings reveal a TRIF-CD40-Th17 axis in the development of IL-17-associated, neutrophilic asthma.
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Mucosal+Immunol 2015 ; 8 (1): 186-97
