Interleukin-4 receptor signaling pathways in asthma pathogenesis

Trends Mol Med. 2004 Oct;10(10):493-9. doi: 10.1016/j.molmed.2004.08.004.

Abstract

Asthma is a chronic allergic inflammatory disease, the initiation and progression of which is dependent on the cytokines interleukin (IL)-4 and IL-13 acting through related receptor complexes. Disease pathogenesis is effected by intracellular signaling pathways that couple primarily to specific motifs within the intracellular domain of the IL-4 receptor alpha chain (IL-4Ralpha), a subunit that is common to the IL-4 and IL-13 receptor complexes. Recent studies using genetic approaches have identified distinct functions for the respective IL-4Ralpha-coupled signaling pathways in regulating both early and chronic stages of asthma. Polymorphisms in components of the IL-4 and IL-13 cytokine-receptor axes are associated with allergy and asthma, suggesting that variations among individuals in the activity of this pathway contribute to disease susceptibility and manifestations.

Publication types

  • Review

MeSH terms

  • Animals
  • Asthma / etiology*
  • Asthma / immunology
  • Asthma / metabolism
  • DNA-Binding Proteins / metabolism
  • Humans
  • Hypersensitivity / immunology
  • Interleukin-13 / genetics
  • Interleukin-13 / metabolism
  • Interleukin-4 Receptor alpha Subunit
  • Mice
  • Models, Molecular
  • Polymorphism, Genetic
  • Receptors, Cell Surface
  • Receptors, Interleukin-4 / genetics
  • Receptors, Interleukin-4 / metabolism*
  • STAT6 Transcription Factor
  • Signal Transduction*
  • Trans-Activators / metabolism

Substances

  • DNA-Binding Proteins
  • IL4R protein, human
  • Il4ra protein, mouse
  • Interleukin-13
  • Interleukin-4 Receptor alpha Subunit
  • Receptors, Cell Surface
  • Receptors, Interleukin-4
  • STAT6 Transcription Factor
  • STAT6 protein, human
  • Trans-Activators