Requirement for IL-13 independently of IL-4 in experimental asthma

被引:1612
作者
Grünig, G
Warnock, M
Wakil, AE
Venkayya, R
Brombacher, F
Rennick, DM
Sheppard, D
Mohrs, M
Donaldson, DD
Locksley, RM
Corry, DB [1 ]
机构
[1] Univ Calif San Francisco, San Francisco Gen Hosp, Dept Med, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, San Francisco Gen Hosp, Dept Lung Biol, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA
[4] Calif Pacific Med Ctr, Dept Transplantat, San Francisco, CA 94115 USA
[5] Univ Cape Town, Groote Schuur Hosp, Dept Immunol, ZA-7700 Rondebosch, South Africa
[6] DNAX Res Inst Mol & Cellular Biol Inc, Palo Alto, CA 94304 USA
[7] Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
[8] Univ Calif San Francisco, Dept Immunol Microbiol, San Francisco, CA 94143 USA
[9] Genet Inst, Cambridge, MA 02140 USA
关键词
D O I
10.1126/science.282.5397.2261
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The pathogenesis of asthma reflects, in part, the activity of T cell cytokines. Murine models support participation of interleukin-4 (IL-4) and the IL-4 receptor in asthma. Selective neutralization of IL-13, a cytokine related to IL-4 that also binds to the alpha chain of the IL-4 receptor, ameliorated the asthma phenotype, including airway hyperresponsiveness, eosinophil recruitment, and mucus overproduction. Administration of either IL-13 or IL-4 conferred an asthma-like phenotype to nonimmunized T cell-deficient mice by an IL-4 receptor alpha chain-dependent pathway. This pathway may underlie the genetic associations of asthma with both the human 5q31 Locus and the IL-4 receptor.
引用
收藏
页码:2261 / 2263
页数:3
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