The inflammatory diseases ulcerative colitis and Crohn's disease constitute the 
two main forms of inflammatory bowel disease (IBD). They are characterized by 
chronic, relapsing inflammation of the gastrointestinal tract, significantly 
impacting on patient quality of life and often requiring prolonged treatment. 
Existing therapies for IBD are not effective for all patients, and an unmet need 
exists for additional therapies to induce and maintain remission. Here we 
describe the mechanism of action of the Janus kinase (JAK) inhibitor, 
tofacitinib, for the treatment of IBD and the effect of JAK inhibition on the 
chronic cycle of inflammation that is characteristic of the disease. The 
pathogenesis of IBD involves a dysfunctional response from the innate and 
adaptive immune system, resulting in overexpression of multiple inflammatory 
cytokines, many of which signal through JAKs. Thus JAK inhibition allows 
multiple cytokine signaling pathways to be targeted and is expected to modulate 
the innate and adaptive immune response in IBD, thereby interrupting the cycle 
of inflammation. Tofacitinib is an oral, small molecule JAK inhibitor that is 
being investigated as a targeted immunomodulator for IBD. Clinical development 
of tofacitinib and other JAK inhibitors is ongoing, with the aspiration of 
providing new treatment options for IBD that have the potential to deliver 
prolonged efficacy and clinically meaningful patient benefits.