STAT6 expression in T cells, alveolar macrophages and bronchial biopsies of normal and asthmatic subjects. 2012

Katsuyuki Tomita, and Gaetano Caramori, and Kazuhiro Ito, and Hiroyuki Sano, and Sam Lim, and Timothy Oates, and Borja Cosio, and K Fan Chung, and Yuji Tohda, and Peter J Barnes, and Ian M Adcock
Department of Respiratory Medicine and Allergology, Kinki University School of Medicine, Osaka, Japan.

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.

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