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Muc5ac is required for IL-4 and IL-13-mediated signaling through the type II IL-4 receptor complex

Thursday, October 11, 2012 — Poster Session IV

2:00 p.m. – 4:00 p.m.

Natcher Conference Center, Building 45



* FARE Award Winner


  • K.N. Kindrachuk
  • T.R. Ramalingam
  • M.M. Mentink-Kane
  • L. Barron
  • K.M. Vannella
  • J. Kindrachuk
  • S. White
  • C. DeClercq
  • C. Williams
  • C. Hubeau
  • A. Cheever
  • C.M. Evans
  • T.A. Wynn


Secreted mucins are large complex glycoproteins that determine the dynamic viscoelastic properties of mucus. MUC5AC is a secreted mucin produced by goblet cells of the airway epithelium and is the predominant mucin in the lungs of individuals with allergic asthma. Upregulation of MUC5AC in allergic airways is largely mediated by the type-2 cytokine IL-13, the cytokine responsible for driving much of the pathology associated with allergic asthma. Here, we show that mice deficient in Muc5ac develop airway eosinophilia or mucus cell metaplasia in three models of type-2-mediated lung inflammation. Mechanistically, we demonstrate that Muc5ac is required for type-2 cytokine signaling via the IL13Rα1 chain of the type II IL-4 receptor and that this effect is cell intrinsic and thus not due to secreted Muc5ac. This work uncovers a novel and essential role for Muc5ac in controlling the pathology of allergic asthma and other Th2-mediated diseases.

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