Аннотация:BackgroundInflammatory Bowel Disease (IBD) is a chronic inflammatory condition characterized by unrestrained inflammation. Regulatory T cell (Tregs) mediated suppression of this overactive immune response is impaired in IBD patients suggesting that strategies to improve Treg function may offer therapeutic potential. We have previously shown that inhibition of heat shock protein 90 attenuates inflammation in murine models through increased nuclear translocation of the transcription factor heat shock factor 1 (HSF1). Based on these findings we hypothesized that pharmacological activation of HSF1 might exert similar anti-inflammatory properties in murine IBD models.
