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Blanchard, Carine; Wang, Ning; Stringer, Keith F; Mishra, Anil; Fulkerson, Patricia C; Abonia, J Pablo; Jameson, Sean C; Kirby, Cassie; Konikoff, Michael R; Collins, Margaret H; Cohen, Mitchell B; Akers, Rachel; Hogan, Simon P; Assa'ad, Amal H; Putnam, Philip E; Aronow, Bruce J; Rothenberg, Marc E
The Journal of clinical investigation, 02/2006, Letnik: 116, Številka: 2Journal Article
Eosinophilic esophagitis (EE) is an emerging disorder with a poorly understood pathogenesis. In order to define disease mechanisms, we took an empirical approach analyzing esophageal tissue by a genome-wide microarray expression analysis. EE patients had a striking transcript signature involving 1% of the human genome that was remarkably conserved across sex, age, and allergic status and was distinct from that associated with non-EE chronic esophagitis. Notably, the gene encoding the eosinophil-specific chemoattractant eotaxin-3 (also known as CCL26) was the most highly induced gene in EE patients compared with its expression level in healthy individuals. Esophageal eotaxin-3 mRNA and protein levels strongly correlated with tissue eosinophilia and mastocytosis. Furthermore, a single-nucleotide polymorphism in the human eotaxin-3 gene was associated with disease susceptibility. Finally, mice deficient in the eotaxin receptor (also known as CCR3) were protected from experimental EE. These results implicate eotaxin-3 as a critical effector molecule for EE and provide insight into disease pathogenesis.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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