Interleukin 9: A candidate gene for asthma

Nicholas C. Nicolaides; Kenneth J. Holroyd; Susan L. Ewart; Scott M. Eleff; Matthew B. Kiser; Carl R. Dragwa; Christine D. Sullivan; Luigi Grasso; Liu Yi Zhang; Carol J. Messler; Tingyi Zhou; Steven R. Kleeberger; Kenneth H. Buetow; Roy C. Levitt

doi:10.1073/pnas.94.24.13175

Interleukin 9: A candidate gene for asthma

Nicholas C. Nicolaides, Kenneth J. Holroyd, Susan L. Ewart, Scott M. Eleff, Matthew B. Kiser, Carl R. Dragwa, Christine D. Sullivan, Luigi Grasso, Liu Yi Zhang, Carol J. Messler, Tingyi Zhou, Steven R. Kleeberger, Kenneth H. Buetow, Roy C. Levitt

Research output: Contribution to journal › Article › peer-review

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Abstract

Asthma is a complex heritable inflammatory disorder of the airways associated with clinical signs of atopy and bronchial hyperresponsiveness. Recent studies localized a major gene for asthma to chromosome 5q31-q33 in humans. Thus, this segment of the genome represents a candidate region for genes that determine susceptibility to bronchial hyperresponsiveness and atopy in animal models. Homologs of candidate genes on human chromosome 5q31- q33 are found in four regions in the mouse genome, two on chromosome 18, and one each on chromosomes 11 and 13. We assessed bronchial responsiveness as a quantitative trait in mice and found it linked to chromosome 13. Interleukin 9 (IL-9) is located in the linked region and was analyzed as a gene candidate. The expression of IL-9 was markedly reduced in bronchial hyporesponsive mice, and the level of expression was determined by sequences within the qualitative trait locus (QTL). These data suggest a role for IL-9 in the complex pathogenesis of bronchial hyperresponsiveness as a risk factor for asthma.

Original language	English (US)
Pages (from-to)	13175-13180
Number of pages	6
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	94
Issue number	24
DOIs	https://doi.org/10.1073/pnas.94.24.13175
State	Published - Nov 25 1997
Externally published	Yes

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Nicolaides, N. C., Holroyd, K. J., Ewart, S. L., Eleff, S. M., Kiser, M. B., Dragwa, C. R., Sullivan, C. D., Grasso, L., Zhang, L. Y., Messler, C. J., Zhou, T., Kleeberger, S. R., Buetow, K. H., & Levitt, R. C. (1997). Interleukin 9: A candidate gene for asthma. Proceedings of the National Academy of Sciences of the United States of America, 94(24), 13175-13180. https://doi.org/10.1073/pnas.94.24.13175

Nicolaides, NC, Holroyd, KJ, Ewart, SL, Eleff, SM, Kiser, MB, Dragwa, CR, Sullivan, CD, Grasso, L, Zhang, LY, Messler, CJ, Zhou, T, Kleeberger, SR, Buetow, KH & Levitt, RC 1997, 'Interleukin 9: A candidate gene for asthma', Proceedings of the National Academy of Sciences of the United States of America, vol. 94, no. 24, pp. 13175-13180. https://doi.org/10.1073/pnas.94.24.13175

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abstract = "Asthma is a complex heritable inflammatory disorder of the airways associated with clinical signs of atopy and bronchial hyperresponsiveness. Recent studies localized a major gene for asthma to chromosome 5q31-q33 in humans. Thus, this segment of the genome represents a candidate region for genes that determine susceptibility to bronchial hyperresponsiveness and atopy in animal models. Homologs of candidate genes on human chromosome 5q31- q33 are found in four regions in the mouse genome, two on chromosome 18, and one each on chromosomes 11 and 13. We assessed bronchial responsiveness as a quantitative trait in mice and found it linked to chromosome 13. Interleukin 9 (IL-9) is located in the linked region and was analyzed as a gene candidate. The expression of IL-9 was markedly reduced in bronchial hyporesponsive mice, and the level of expression was determined by sequences within the qualitative trait locus (QTL). These data suggest a role for IL-9 in the complex pathogenesis of bronchial hyperresponsiveness as a risk factor for asthma.",

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AU - Messler, Carol J.

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AU - Buetow, Kenneth H.

AU - Levitt, Roy C.

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Interleukin 9: A candidate gene for asthma

Abstract

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