Conflicts of interest None declared.
The role of T-cell reactivity towards the autoantigen α-NAC in atopic dermatitis
Article first published online: 28 JAN 2011
© 2011 The Authors. BJD © 2011 British Association of Dermatologists
British Journal of Dermatology
Volume 164, Issue 2, pages 316–324, February 2011
How to Cite
Heratizadeh, A., Mittermann, I., Balaji, H., Wichmann, K., Niebuhr, M., Valenta, R. and Werfel, T. (2011), The role of T-cell reactivity towards the autoantigen α-NAC in atopic dermatitis. British Journal of Dermatology, 164: 316–324. doi: 10.1111/j.1365-2133.2010.10090.x
Funding sources This study was supported in part by grants GRK1441 and SFB566 A6 of the Deutsche Forschungsgemeinschaft and by grant F1815 of the Austrian Science Fund.
- Issue published online: 28 JAN 2011
- Article first published online: 28 JAN 2011
- Accepted manuscript online: 25 OCT 2010 11:55PM EST
- Accepted for publication 12 October 2010
Background A subgroup of patients with atopic dermatitis (AD) produces IgE autoantibodies to human proteins which may be present in inflamed skin and perpetuate cutaneous inflammation.
Objectives In order to investigate mechanisms of ‘autoallergy’ for AD we studied T-cell responses to the autoallergen Hom s 2, the human transcriptional coactivator α-nascent polypeptide-associated complex (α-NAC).
Methods Specific proliferation of blood lymphocytes from 30 patients and 12 healthy control individuals was investigated by flow cytometry. The proliferation of skin- and blood-derived T cells was assessed in limiting-dilution assays. T-cell clones (TCC) were generated from peripheral blood and from biopsies of lesional skin of patients with AD and the phenotype and cytokine patterns were determined.
Results α-NAC-specific T-cell responses were detected in patients and control individuals. α-NAC induced a significantly higher proliferation of CCR4+ (compared with CCR4−) and CLA+ (compared with CLA−) T cells from the circulation. Limiting-dilution assays revealed a high proliferation of blood and skin-infiltrating lymphocytes in the presence of α-NAC compared with control cultures. α-NAC-specific TCC generated from lesional skin of AD predominantly produced interferon-γ and some TCC also produced interleukin-17. The cytokine pattern of α-NAC TCC may contribute to keratinocyte apoptosis and eczema formation in AD.
Conclusions α-NAC-specific TCC can be generated from blood and lesional skin of patients with AD. These TCC produce not only Th2 but also Th1 cytokines which may explain the Th1 phenotype of inflammation in AD.