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This article is part of the supplement: 25th European Workshop for Rheumatology Research

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Gene expression in chronically activated Th cells

U Niesner1, I Albrecht1, R Baumgrass1, M Janitz2, H Lehrach2, T Haeupl3, J Grun4, GR Burmester3, A Grutzkau1 and A Radbruch1

Author Affiliations

1 German Arthritis Research Centre, Berlin, Germany

2 Department of Vertebrate Genomics, Max Planck Institute for Molecular Genetics, Berlin, Germany

3 Department of Rheumatology and Clinical Immunology, Charité University Medical Centre, Berlin, Germany

4 Oligene Inc., Berlin, Germany

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Arthritis Research & Therapy 2005, 7(Suppl 1):P90  doi:10.1186/ar1611

The electronic version of this article is the complete one and can be found online at:

Received:11 January 2005
Published:17 February 2005

© 2005 BioMed Central Ltd

Poster presentation

Th lymphocytes are considered to be key players in chronic inflammation. Upon repeated re-stimulation and differential instruction, they can develop a stable memory for the expression of distinct genes coding for cytokines, chemokines, adhesion molecules, and so on. This functional memory contributes considerably to the chronicity of inflammation and its eventual refraction to therapy.

Here, we describe the global gene expression profiles of in vitro repeatedly reactivated murine Th1 and Th2 cells, and compare them with those of naïve and once activated Th1 and Th2 cells, both before and after re-stimulation (Fig. 1).

Among differentially expressed genes is a novel transcription factor, which down-modulates NF-κB signalling and is exclusively expressed in repeatedly re-activated Th1 cells. High expression of this gene can be detected in Th cells isolated from the site of inflammation of patients suffering from distinct forms of rheumatic diseases or ulcerative colitis, but not in Th cells isolated from healthy tissue or from blood.

Expression of this gene in Th cells at the site of inflammation highlights the role of chronic T-cell activation in chronic inflammation and may represent an endogenous mechanism to limit inflammation. Apart from its diagnostic value, this molecular pathway also points to a new therapeutic target.

thumbnailFigure 1. Hierarchical clustering of differentially expressed genes among doublets of the nine investigated cell populations (w, weeks in culture; res, 3 hours re-stimulated) using Affymetrix Mouse Genome 430A 2.0 Arrays and DNA-Chip Analyzer (dChip).