Fig. 5.

Model of enhanced pro-inflammatory cytokine production by ER stress-induced inhibition of IL-10 signaling. In the absence of ER stress, IL-10 potently inhibits PRR-induced cytokine production through recognition by the IL-10 receptor and subsequent STAT3 Tyr705 phosphorylation leading to SOCS3 production. In contrast, when cells are undergoing ER stress, STAT3 Tyr705 phosphorylation is inhibited, resulting in abrogation of the immunosuppressive effect of IL-10 and increased pro-inflammatory cytokine production