Role of ER stress in inflammation
Our work has identified that the response of innate immune cells to pathogens can be modified by the activation of cellular stress pathways. This was clearly shown by the requirement for the ER stress induced transcription factor, CHOP, in the expression of the pro-inflammatory cytokine, IL-23. We are currently embarking on a 5 year research programme funded by Arthritis UK, to investigate whether collagen induced arthritis (an inflammatory condition that is highly dependent on IL-23) can be modulated by changes in the quality of the ER stress response.
Goodall, JC., Changxin W., Zhang, Y., Ellis, L. O’Brien., L. Saudek, V and Gaston, JSH. ER stress signals are integrated by dendritic cells to enhance IL-23 responses to Toll-like receptor . PNAS, 12;107(41):17698-703