Importance of cytokines in murine allergic airway disease and human asthma

J Immunol. 2010 Feb 15;184(4):1663-74. doi: 10.4049/jimmunol.0902185.

Abstract

Asthma is a common, disabling inflammatory respiratory disease that has increased in frequency and severity in developed nations. We review studies of murine allergic airway disease (MAAD) and human asthma that evaluate the importance of Th2 cytokines, Th2 response-promoting cytokines, IL-17, and proinflammatory and anti-inflammatory cytokines in MAAD and human asthma. We discuss murine studies that directly stimulate airways with specific cytokines or delete, inactivate, neutralize, or block specific cytokines or their receptors, as well as controversial issues including the roles of IL-5, IL-17, and IL-13Ralpha2 in MAAD and IL-4Ralpha expression by specific cell types. Studies of human asthmatic cytokine gene and protein expression, linkage of cytokine polymorphisms to asthma, cytokine responses to allergen stimulation, and clinical responses to cytokine antagonists are discussed as well. Results of these analyses establish the importance of specific cytokines in MAAD and human asthma and have therapeutic implications.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Allergens / administration & dosage
  • Allergens / immunology*
  • Animals
  • Asthma / genetics
  • Asthma / immunology*
  • Asthma / pathology
  • Asthma / prevention & control
  • Cytokines / antagonists & inhibitors
  • Cytokines / biosynthesis
  • Cytokines / genetics
  • Cytokines / physiology*
  • Disease Models, Animal
  • Humans
  • Inflammation Mediators / antagonists & inhibitors
  • Inflammation Mediators / metabolism
  • Inflammation Mediators / physiology
  • Mice
  • Respiratory Hypersensitivity / genetics
  • Respiratory Hypersensitivity / immunology*
  • Respiratory Hypersensitivity / pathology
  • Respiratory Hypersensitivity / therapy

Substances

  • Allergens
  • Cytokines
  • Inflammation Mediators