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Volume 120, Issue 3, Pages 544-550 (September 2007)


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Advances in asthma, allergy mechanisms, and genetics in 2006

Fred D. Finkelman, MDa, Donata Vercelli, MDbCorresponding Author Informationemail address

Received 7 May 2007; received in revised form 8 May 2007; accepted 11 May 2007. published online 05 July 2007.

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.

a Division of Immunology, University of Cincinnati, Cincinnati, Ohio

b Arizona Respiratory Center, University of Arizona Health Sciences Center, Tucson, Ariz

Corresponding Author InformationReprint requests: Donata Vercelli, Arizona Respiratory Center, University of Arizona Health Sciences Center, 1501 N Campbell Ave, Suite 2349, Tucson, AZ 85724-5030.

 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.

PII: S0091-6749(07)00992-X

doi:10.1016/j.jaci.2007.05.025


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