Functional Importance of Regional Differences in Localized Gene Expression of Receptors for IL-13 in Murine Gut

IL-13 induces a STAT6-dependent hypercontractility of intestinal smooth muscle that is mediated by binding to the IL-13Ralpha1 component of the type 2 IL-4R that is linked to STAT6. IL-13 also binds to the IL-13Ralpha2 that is not linked to STAT6 and functions to limit the effects of IL-13 in vivo....

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Veröffentlicht in:Journal of Immunology 2006-01, Vol.176 (1), p.491-495
Hauptverfasser: Morimoto, Motoko, Morimoto, Masahiro, Zhao, Aiping, Madden, Kathleen B, Dawson, Harry, Finkelman, Fred D, Mentink-Kane, Margaret, Urban, Joseph F., Jr, Wynn, Thomas A, Shea-Donohue, Terez
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Sprache:eng
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Zusammenfassung:IL-13 induces a STAT6-dependent hypercontractility of intestinal smooth muscle that is mediated by binding to the IL-13Ralpha1 component of the type 2 IL-4R that is linked to STAT6. IL-13 also binds to the IL-13Ralpha2 that is not linked to STAT6 and functions to limit the effects of IL-13 in vivo. In this study we assessed the contributions of regional and cellular differences in the distribution of the IL-13R components to the physiological regulation of smooth muscle function in wild-type mice and mice deficient in STAT6 or IL-13Ralpha2. The expression of IL-13 and IL-13Ralpha2 was higher in colon than in small intestine. Laser capture microdissection of specific cell types revealed that the expression of IL-13Ralpha2 was higher in the smooth muscle layer compared with levels in the epithelial cells of the mucosa. In contrast, there was a uniform distribution of IL-13alpha1 in smooth muscle, epithelia, and myenteric neurons. The significant hypercontractility of smooth muscle in mice deficient in IL-13Ralpha2, but not in STAT6, shows the physiological importance of IL-13 binding to IL-13Ralpha2. The pronounced differences in the expression of IL-13Ralpha2 suggest that the gut has developed sophisticated mechanisms for controlling the physiological and pathophysiological activities of IL-13.
ISSN:0022-1767
1550-6606
1365-2567
DOI:10.4049/jimmunol.176.1.491