The online version of this article (doi:10.1186/1476-9255-9-5) contains supplementary material, which is available to authorized users.
Katsuyuki Tomita, Gaetano Caramori contributed equally to this work.
The authors declare that they have no competing interests.
KT and GC: Conceived & designed the study & drafted the manuscript. IK, SL and HS: Helped design & participated in the clinical studies & drafting the manuscript. TQ: Participated in the immunohistochemical studies. SL and BC: Helped in clinical samples. KF, YT, PB, and IA: Participated in the study design & coordination and drafting of the manuscript. All authors read and approved the final manuscript.
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.
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- STAT6 expression in T cells, alveolar macrophages and bronchial biopsies of normal and asthmatic subjects
K Fan Chung
Peter J Barnes
Ian M Adcock
- BioMed Central
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