Advances in asthma, allergy mechanisms, and genetics in 2006

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 T_H2 response and in determining how T_H2 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.

Key words: Allergy, asthma, mechanisms, mouse models, genetics, single nucleotide polymorphisms, association studies, linkage studies

Abbreviations used: AAD, Allergic airway disease, ADAMTS12, A disintegrin and metalloproteinase domain with thrombospondin type 1 motif 12, AHR, Airway hyperresponsiveness, AOAH, Acyloxyacyl hydroxylase, BHR, Bronchial hyperresponsiveness, DC, Dendritic cell, ESR, Estrogen receptor, IL-7R, IL-7 receptor, LIFR, Leukemia inhibitory factor receptor, PTGDR, Prostanoid DP receptor, PTGER4, Prostaglandin E4 receptor, SNP, Single nucleotide polymorphism, STAT, Signal transducer and activator of transcription, TLR, Toll-like receptor, VEGF, Vascular endothelial growth factor, ZFR, Zinc finger RNA binding protein