Volume 8 Supplement 1

5th European Workshop on Immune-Mediated Inflammatory Diseases

Open Access

Expression of IL-1 family members upon stimulation with IL-17 differs in keratinocytes derived from psoriasis patients and healthy donors

  • P Muhr1,
  • J Zeitvogel1,
  • T Werfel1 and
  • M Wittmann1, 2
Contributed equally
Journal of Translational Medicine20108(Suppl 1):P19

https://doi.org/10.1186/1479-5876-8-S1-P19

Published: 25 November 2010

Background

A number of studies have challenged the T cell centred pathogenetic view of psoriasis by the finding that epithelium-expressed genes are intimately involved in the inflammatory process. IL-17 is an important inflammatory mediator in skin psoriasis.

Objective

IL-17 is known to act on keratinocytes and we were interested in its impact on expression of pro- and anti-inflammatory IL-1 family members.

Methods

We compared human primary keratinocytes derived from psoriasis patients and healthy individuals using qRT-PCR and ELISA.

Results

In the presence of IL-17 psoriasis derived keratinocytes showed a significantly higher induction of the pro-inflammatory members IL-1F6 and IL-1F9 compared with those from healthy individuals but not of anti-inflammatory members IL-1F5, IL-1F7 or IL-1F3. Both basal, as well as IL-17 induced production of IL-1F2/IL-1β and IL-1F1/IL-1α were found to be significantly lower in psoriasis keratinocytes.

Conclusion

As keratinocytes were derived from epidermal stem cells of the hair follicles and obtained from non-lesional sites, differences found are likely to present an intrinsic feature of psoriasis epithelium. Our data suggest that the significance of IL-1 members as therapeutic targets in psoriasis conditions merits further and thorough investigation.

Notes

Authors’ Affiliations

(1)
Dept. of Dermatology and Allergy, Division of Immunodermatology and Allergy Research, Hannover Medical School
(2)
Institute of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds

Copyright

© Wittmann et al; licensee BioMed Central Ltd. 2010

This article is published under license to BioMed Central Ltd.

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