JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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MyD88 modulates eosinophil and neutrophil recruitment as well as IL-17A production during allergic inflammation.

Cellular Immunology 2016 December
The contribution of dysregulated innate immune responses to the pathogenesis of allergic disease remains largely unknown. Herein, we addressed the role of Toll-like receptor signaling in airway inflammation by studying mice rendered deficient for the myeloid differentiation factor 88 (MyD88-/-) which results in concurrent deficiencies in TLR and IL-1R1 signaling pathways. We show that the lack of MyD88 offers a partial protection from allergic disease evidenced by reduced airway eosinophilia and production of the Th17-associated effector cytokine IL-17A. By contrast, airway hyperreactivity and Th2 cytokine production, the cardinal features of allergic disease, remained unchanged. We found that the impaired IL-17A production in MyD88-/- mice was associated with defective CD4+ T cells, which failed to respond to IL-23 stimulation. The total number of Th17-associated effectors in lymph nodes was likewise decreased. Taken together, our results demonstrate that MyD88-dependent mechanisms are critical for orchestrating lung inflammatory responses, in terms of IL-17A production, as well as eosinophil and neutrophil recruitment.

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