| First Author | Seki Y | Year | 2003 |
| Journal | Nat Med | Volume | 9 |
| Issue | 8 | Pages | 1047-54 |
| PubMed ID | 12847520 | Mgi Jnum | J:84845 |
| Mgi Id | MGI:2670322 | Doi | 10.1038/nm896 |
| Citation | Seki Y, et al. (2003) SOCS-3 regulates onset and maintenance of T(H)2-mediated allergic responses. Nat Med 9(8):1047-54 |
| abstractText | 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 (T(H)2) cells, but its role in T(H)2-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 T(H)2 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 T(H)2 development. These data indicate that SOCS-3 has an important role in regulating the onset and maintenance of T(H)2-mediated allergic immune disease, and suggest that SOCS-3 may be a new therapeutic target for the development of antiallergic drugs. |
