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

Katsuyuki Tomita1*, Gaetano Caramori23, Kazuhiro Ito3, Hiroyuki Sano1, Sam Lim3, Timothy Oates3, Borja Cosio3, K Fan Chung3, Yuji Tohda1, Peter J Barnes3 and Ian M Adcock3

Author Affiliations

1 Department of Respiratory Medicine and Allergology, Kinki University School of Medicine, Osaka, Japan

2 Section of Respiratory Diseases, Department of Clinical and Experimental Medicine, Università di Ferrara, Ferrara, Italy

3 Airway Disease Section, National Heart and Lung Institute, Imperial College of London, London, UK

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Journal of Inflammation 2012, 9:5  doi:10.1186/1476-9255-9-5

Published: 9 March 2012



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.


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.


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.


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.

Airway epithelial cells; Alveolar macrophages; Asthma; STAT6; T-cells; Th2 cells