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

被引：1604

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

来源：

SCIENCE | 1998年 / 282卷 / 5397期

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

页码：2261 / 2263

页数：3

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