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STAT6 expression in T cells, alveolar macrophages and bronchial biopsies of normal and asthmatic subjects

BACKGROUND: Asthma is characterised by increased numbers of Th2-like cells in the airways and IgE secretion. Generation of Th2 cells requires interleukin (IL)-4 and IL-13 acting through their specific receptors and activating the transcription factor, signal transducer and activator of transcription...

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Detalles Bibliográficos
Autores principales: Tomita, Katsuyuki, Caramori, Gaetano, Ito, Kazuhiro, Sano, Hiroyuki, Lim, Sam, Oates, Timothy, Cosio, Borja, Chung, K Fan, Tohda, Yuji, Barnes, Peter J, Adcock, Ian M
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3364916/
https://www.ncbi.nlm.nih.gov/pubmed/22401596
http://dx.doi.org/10.1186/1476-9255-9-5
Descripción
Sumario:BACKGROUND: Asthma is characterised by increased numbers of Th2-like cells in the airways and IgE secretion. Generation of Th2 cells requires interleukin (IL)-4 and IL-13 acting through their specific receptors and activating the transcription factor, signal transducer and activator of transcription 6 (STAT6). STAT6 knockout mice fail to produce IgE, airway hyperresponsiveness and bronchoalveolar lavage eosinophilia after allergen sensitisation, suggesting a critical role for STAT6 in allergic responses. METHODS: We have investigated the expression of STAT6 in peripheral blood T-lymphocytes, alveolar macrophages and bronchial biopsies from 17 normal subjects and 18 mild-moderate steroid-naïve stable asthmatic patients. RESULTS: STAT6 expression was variable and was detected in T-lymphocytes, macrophages and bronchial epithelial cells from all subjects with no difference between normal and stable asthmatic subjects. CONCLUSIONS: STAT6 expression in different cells suggests that it may be important in regulating the expression of not only Th2-like cytokines in T cells of man, but may also regulate STAT-inducible genes in alveolar macrophages and airway epithelial cells.