Abstract
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.
Original language | English |
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Pages (from-to) | 1047-1054 |
Number of pages | 8 |
Journal | Nature medicine |
Volume | 9 |
Issue number | 8 |
DOIs | |
Publication status | Published - Aug 1 2003 |
Externally published | Yes |
All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)