| First Author | Miyata S | Year | 1999 |
| Journal | Clin Exp Allergy | Volume | 29 |
| Issue | 1 | Pages | 114-23 |
| PubMed ID | 10051710 | Mgi Jnum | J:103165 |
| Mgi Id | MGI:3608576 | Doi | 10.1046/j.1365-2222.1999.00405.x |
| Citation | Miyata S, et al. (1999) STAT6 deficiency in a mouse model of allergen-induced airways inflammation abolishes eosinophilia but induces infiltration of CD8+ T cells. Clin Exp Allergy 29(1):114-23 |
| abstractText | BACKGROUND: The TH2-type cytokines have been reported to contribute to the asthmatic response. STAT6 has an essential role in IL-4 signalling and in production of TH2 cytokines from T cells and is involved in IgE and IgG1 responses after nematode infections, indicating that STAT6 has an important role in allergic diseases. OBJECTIVE: In this study we investigated the effects of STAT6 deficiency on allergen-induced airways inflammation in mice. METHODS: Both ovalbumin (OVA)-sensitized STAT6 deficient (STAT6-/-) mice and wild-type C57BL/6 mice were challenged with aerosolized OVA. Changes in inflammatory cell infiltration and cytokine levels in lung tissue as well as serum immunoglobulin levels were analysed in OVA-challenged STAT6-/- and wild-type mice. RESULTS: The eosinophilia and lung damage normally resulting from aeroallergen challenge were not seen in STAT6-/- mice. Expression of TH2 cytokines (IL-4 and IL-5) in the lung tissue as well as IgE and IgG1 responses after OVA challenge were profoundly reduced in STAT6-/- mice, whereas expression of IFNgamma was the same in STAT6-/- mice and wild-type mice after OVA challenge. Immunocytochemical analysis of T cells showed the infiltration of CD4+ T cells but not CD8+ T cells increased into the lung of wild-type mice after OVA challenge. However, the OVA-exposed STAT6-/- mice demonstrated the infiltration of both CD4+ T cells and CD8+ T cells with a significant increase in percentage and total number of CD8+ T cells compared with OVA-exposed wild-type mice. CONCLUSION: These results indicate that factors which signal through STAT6 are important regulators of eosinophilia of allergic airway inflammation, regulating TH2-type cytokine production both in CD4+ T cells and CD8+ T cells. |
