Emerging pathways in asthma: innate and adaptive interactions

Biochim Biophys Acta. 2011 Nov;1810(11):1052-8. doi: 10.1016/j.bbagen.2011.04.015. Epub 2011 May 5.

Abstract

Background: Allergic asthma is a complex and chronic airway inflammatory disorder, and the prevalence of asthma has increased. Adaptive antigen-dependent immunity is a classical pathway of asthmatic pathology. Recent studies have focused on innate antigen-independent immunity in asthma.

Scope of review: This review discusses updated research associating innate immunity with allergic asthma. We focus on innate molecules (Toll-like receptors and nucleotide-binding oligomerization domain-like receptors) and review studies regarding innate and adaptive interactions in allergic responses (surfactant protein D, lipopolysaccharide, and early life immune responses). We also highlight new emerging concepts in the field applicable to innate immunity and asthma.

Major conclusions: Innate immunity plays a key role in asthma. Understanding innate and adaptive interactions provide significant information in asthmatic research. Innate molecules not only contribute to classical pulmonary defense, but also modulate inflammatory responses. Emerging concepts in the analysis of the microbiome, microRNA and autophagy may provide new insights in searching therapeutic targets.

General significance: Finding specific mechanisms of innate and/or adaptive immunity in asthma are timely goals for further research. Integration of bioinformatics and systems biology tools, particularly in relation to microbiome analysis, may be helpful in providing an understanding to allergic immune responses. This article is part of a Special Issue entitled Biochemistry of Asthma.

Publication types

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

MeSH terms

  • Adaptive Immunity
  • Animals
  • Asthma / drug therapy
  • Asthma / etiology
  • Asthma / immunology*
  • Humans
  • Immunity, Innate
  • Nod2 Signaling Adaptor Protein / physiology
  • Toll-Like Receptors / physiology

Substances

  • NOD2 protein, human
  • Nod2 Signaling Adaptor Protein
  • Toll-Like Receptors