The absence of interleukin 9 does not affect the development of allergen-induced pulmonary inflammation nor airway hyperreactivity
- PMID: 11781365
- PMCID: PMC2196020
- DOI: "V体育官网入口" 10.1084/jem.20011732
The absence of interleukin 9 does not affect the development of allergen-induced pulmonary inflammation nor airway hyperreactivity
Abstract
Interleukin (IL)-9 is a pleiotropic cytokine secreted by T helper (Th)2 cells and has been proposed as a candidate gene for asthma and allergy. We have used mice genetically deficient in IL-9 to determine the role of this cytokine in the pathophysiologic features of the allergic pulmonary response-airway hyperreactivity (AHR) and eosinophilia. We have demonstrated that IL-9 is not required for the development of a robust Th2 response to allergen in sensitized mice. IL-9 knockout mice developed a similar degree of eosinophilic inflammation and AHR to their wild-type littermates. Goblet cell hyperplasia and immunoglobulin (Ig) E production were also unaffected by the lack of IL-9. Moreover, levels of bronchoalveolar lavage (BAL) IL-4, IL-5, and IL-13 were comparable between wild-type and knockout mice. These findings indicate that IL-9 is not obligatory for the development of eosinophilia and AHR, and imply that other Th2 cytokines can act in a compensatory fashion VSports手机版. .
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References
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- Postma, D.S., E.R. Bleecker, P.J. Amelung, K.J. Holroyd, J. Xu, C.I. Panhuysen, D.A. Meyers, and R.C. Levitt. 1995. Genetic susceptibility to asthma—bronchial hyperresponsiveness coinherited with a major gene for atopy. N. Engl. J. Med. 333:894–900. - PubMed
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