抄録
Members of the suppressor of cytokine signaling (SOCS) family are involved in the pathogenesis of many inflammatory diseases. SOCS-3 is predominantly expressed in T-helper type 2 (TH2) cells, but its role in T H2-related allergic diseases remains to be investigated. In this study we provide a strong correlation between SOCS-3 expression and the pathology of asthma and atopic dermatitis, as well as serum IgE levels in allergic human patients. SOCS-3 transgenic mice showed increased TH2 responses and multiple pathological features characteristic of asthma in an airway hypersensitivity model system. In contrast, dominant-negative mutant SOCS-3 transgenic mice, as well as mice with a heterozygous deletion of Socs3, had decreased TH2 development. These data indicate that SOCS-3 has an important role in regulating the onset and maintenance of T H2-mediated allergic immune disease, and suggest that SOCS-3 may be a new therapeutic target for the development of antiallergic drugs.
本文言語 | 英語 |
---|---|
ページ(範囲) | 1047-1054 |
ページ数 | 8 |
ジャーナル | Nature medicine |
巻 | 9 |
号 | 8 |
DOI | |
出版ステータス | 出版済み - 8月 1 2003 |
!!!All Science Journal Classification (ASJC) codes
- 生化学、遺伝学、分子生物学(全般)