Published ahead of print on February 10, 2006, doi:10.1165/rcmb.2005-0314OC Am. J. Respir. Cell Mol. Biol., Volume 34, Number 6, June 2006, 711-718 A more recent version of this article appeared on June 1, 2006
Submitted on August 17, 2005 Multi-strain Genetic Comparisons Reveal CCR5 as a Receptor Involved in Airway HyperresponsivenessJulia K.L. Walker1*,1 Department of Pulmonary, Allergy and Critical Care Medicine, Duke University Medical Center, Durham, NC, USA, 2 The Institute for Genomic Research, Rockville, MD, USA, 3 Dana-Farber Cancer Institute, Harvard School of Public Health, Boston, MA, USA, 4 The Institute for Genomic Research, Rockville, MD, USA; Dana-Farber Cancer Institute, Harvard School of Public Health, Boston, MA, USA, 5 National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA * To whom correspondence should be addressed. E-mail: walke082{at}mc.duke.edu.
Asthma is a ubiquitous disease with a broad range of clinical phenotypes. To better understand the complex genetic and environmental interactions underlying asthma, we compared the gene-gene interactions of four genetically distinct mouse strains that demonstrate biologically distinct responses to allergen. Using DNA microarrays and knock-out mouse studies, we showed that CCR5 plays a definitive role in the development of ovalbumin-induced allergic airway inflammatory disease. In addition, gene expression profiling data have revealed other potential novel targets for therapeutics-based research and has enhanced the understanding of the molecular mechanisms underlying the etiology of "asthma."
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