Figure 4.

Schematic illustration of the interactions between protein misfolding, the UPR and inflammation. Protein misfolding can be caused by a primary defect, such as a genetic mutation, or can occur as a secondary event as a consequence of microbial ER stressors (for example, bacterial toxins), host ER stressors (for example, hypoxia and increased ATP levels) and/or of inflammation (for example, ROS, cytokines). Misfolding triggers the UPR and NF‐κB activation (Figure 1) activating a network of signalling and transcriptional events that result in increased leukocyte recruitment and T‐cell activation leading to increased inflammation. Inflammation once it develops exacerbates ER stress potentially leading to unresolved cycles of inflammation in susceptible individuals. A full colour version of this figure is available at the Immunology and Cell Biology journal online.