Transcription factors in autoimmune diseases.

The analysis of the molecular basis of autoimmune diseases is currently under intense investigation. The identification of novel mechanisms underlying the pathogenesis of these diseases generates the possibility for the development of new therapeutic agents. In this review we summarize the results leading to novel insights concerning the molecular processes involved in the pathogenesis of rheumatoid arthritis, systemic lupus erythematodes, multiple sclerosis and diabetes type 1.

Expression analysis of the glucocorticoid receptor and the nuclear factor-kB subunit p50 in lymphocytes from patients with rheumatoid arthritis.

Objective: To study a possible relationship between expression of the transcription factor glucocorticoid receptor (GR), which mediates antiinflammatory effects, and the transcription factor p50, which mediates proinflammatory effects, in peripheral blood mononuclear cells (PBMC) of patients with rheumatoid arthritis (RA).

Methods: Expression analysis of GR and nuclear factor-kB subunit p50 in PBMC was performed by semiquantitative immunoblotting.

Results: GR and p50 expression in PBMC were significantly increased in patients with RA who had never received corticosteroids.

Involvement of the glucocorticoid receptor in the pathogenesis of rheumatoid arthritis.

The glucocorticoid receptor (GR) is a ligand-inducible transcription factor which controls the expression of several genes. Its cognate ligand, the glucocorticoids, induces receptor activation by binding to the cytoplasmic located receptor, ultimately leading to translocation of the receptor/hormone complex into the nucleus and the regulation of gene activity. Because glucocorticoids are widely used for suppression of inflammation in rheumatoid arthritis (RA), we investigated whether the expression level of GR is correlated with RA.