Background
We have previously reported on the abnormal expression of the different members of the Jagged/Notch signalling pathway in early rheumatoid arthritis (RA) patients. HES1 and Deltex are two major signalling molecules resulting from the transduction of notch signals. We have shown that signalling through the Jagged/Notch pathway is involved in the development of an anergic phenotype in a T-cell clone model in vitro. We have also used this model to establish a Notch signalling signature characterising a T-cell suppression reaction. We analysed the Notch signature of effecter CD4+ T cells and CD4+CD25high regulatory T cells in RA patients and compared it with healthy controls.