Although it is clear that inflammatory bowel disease (IBD) involves an inappropriate immune response to floral components, the molecular determinants that mediate the gene transcription underlying and aggravating disease remain poorly understood. There is building momentum, however, that implicates differential regulation of the signal transducer and activator of transcription (STAT) 3 as an important factor in mediating pathogenic gene transcription in IBD, and this notion was reinforced by studies presented at the recent 2011 Digestive Disease Week (DDW) conference in Chicago. In the present report we integrate the existing body of literature with the novel data presented at this meeting to present a kaleidoscopic scheme so as to provide further insight into the role of STAT3 in IBD. A genetic propensity to its overactivation in the monocyte and epithelial compartment compromises the innate defense to allow low-level bacterial infection to fester and eventually initiate disease. The subsequent STAT3 activation in various relevant mucosal immune compartments, in particular epithelial cell proliferation and survival, and the function of the regulatory T cells and Th17 cells allow the mucosal immune system to fight the infection and return to steady state. As such, the action of STAT3 in IBD is highly context-dependent but always important.
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