Inflammatory mediators in inflammatory bowel disease

The most important development in the study of the pathogenesis of inflammation in inflammatory bowel disease was the publication of three papers demonstrating that genetically manipulated mice developed chronic intestinal inflammation similar to human inflammatory bowel disease. Two of these genetic models comprised cytokine knockouts (interleukin-2 and interleukin-10), the third model included a series of genetic defects in the T-cell receptor (α and β chains) or the class II major histocompatibility complex. One striking characteristic of these models was the limitation of pathology to the gastrointestinal tract, even though these were all defects in systemic immunity that might have been expected either to cause widespread pathology or to be incompatible with life. The second striking characteristic of these models was the influence of colonic bacteria on the development of pathology.