Reviews and feature articles
Advances in asthma, allergy mechanisms, and genetics in 2006

https://doi.org/10.1016/j.jaci.2007.05.025Get rights and content

This review discusses the main advances in animal models of allergic airway disease and genetics of asthma and allergy published in the Journal in 2006. This work highlighted and extended what has become the central dogma of allergic pathogenesis by highlighting the mechanisms involved in inducing a TH2 response and in determining how TH2 cytokines induce the allergic airway disease phenotype. By so doing, they have identified a considerable number of potential therapeutic targets. Genetic analyses, on the other hand, revealed novel, potentially important candidate genes, confirmed known ones, and refined our understanding of the putative role played by others, sometimes positively, sometimes negatively. These data reiterate allergic inflammation is a classic complex genetic disease—that is, a disorder in which multiple and distinct genetic determinants variously interact with one another and with relevant environmental exposures to result in clinical phenotypes that, although superficially similar, involve distinct genetic pathways and represent the outcome of distinct pathogenetic mechanisms.

Section snippets

From genes to phenotypes and back: 1 year of asthma/allergy genetics in the journal

As recently discussed in these pages,21 allergic reactions involve multiple cellular and molecular interactions that ultimately converge to activate common effector mechanisms of disease. In addition to the classic players such as the TH2 inflammatory pathway, experimental allergy and clinical studies keep highlighting novel molecules and genes, each critical in the context of individual models. In the face of large numbers of studies and models, it is increasingly difficult to gauge the

References (44)

  • T. Tamachi et al.

    IL-25 enhances allergic airway inflammation by amplifying a TH2 cell-dependent pathway in mice

    J Allergy Clin Immunol

    (2006)
  • C.L. Chen et al.

    Serine protease inhibitors nafamostat mesilate and gabexate mesilate attenuate allergen-induced airway inflammation and eosinophilia in a murine model of asthma

    J Allergy Clin Immunol

    (2006)
  • M. Kendall et al.

    Downregulation of IgE antibody and allergic responses in the lung by epidermal biolistic microparticle delivery

    J Allergy Clin Immunol

    (2006)
  • K.S. Lee et al.

    Peroxisome proliferator activated receptor-gamma modulates reactive oxygen species generation and activation of nuclear factor-kappaB and hypoxia-inducible factor 1alpha in allergic airway disease of mice

    J Allergy Clin Immunol

    (2006)
  • A. Munitz et al.

    Reversal of airway inflammation and remodeling in asthma by a bispecific antibody fragment linking CCR3 to CD300a

    J Allergy Clin Immunol

    (2006)
  • S.A. Shore et al.

    Adiponectin attenuates allergen-induced airway inflammation and hyperresponsiveness in mice

    J Allergy Clin Immunol

    (2006)
  • T.J. Ferrara et al.

    Reduced airway hyperresponsiveness and tracheal responses during allergic asthma in mice lacking tyrosine kinase inducible T-cell kinase

    J Allergy Clin Immunol

    (2006)
  • N. Yamashita et al.

    Role of CCL21 and CCL19 in allergic inflammation in the ovalbumin-specific murine asthmatic model

    J Allergy Clin Immunol

    (2006)
  • C. Karagiannidis et al.

    Activin A is an acute allergen-responsive cytokine and provides a link to TGF-beta-mediated airway remodeling in asthma

    J Allergy Clin Immunol

    (2006)
  • A.C. Keller et al.

    Hierarchical suppression of asthma-like responses by mucosal tolerance

    J Allergy Clin Immunol

    (2006)
  • D. Vercelli

    Genetic regulation of IgE responses: Achilles and the tortoise

    J Allergy Clin Immunol

    (2005)
  • D. Vercelli et al.

    The Faustian bargain of genetic association studies: bigger might not be better, or at least it might not be good enough

    J Allergy Clin Immunol

    (2006)
  • Cited by (0)

    Disclosure of potential conflict of interest: D. Vercelli served on the speakers' bureau for Merck. F. D. Finkelman has consultant arrangements with Amgen, Abbott, Plexxikon, Peptimmune, and Wyeth; has patent licensing arrangements with Becton-Dickinson and eBioscience; and has received research support from Amgen and Plexxikon.

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