Recent progresses in basic science have opened new pathogenic scenarios in inflammatory bowel disease. The T helper cell type (Th)1/Th2 paradigm has been outdated thanks to the advances in understanding the function of Th17 cells. Innate immunity, nonimmune cells, and defective tolerogenic mechanisms play a no less crucial role than do adaptive immunity, immune cells, and hyperactivation of effector mechanisms. These new paradigms, together with the no longer "static" but "dynamic" vision of intestinal inflammation, highlight new possible therapeutic targets in inflammatory bowel disease.
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Sabatino et al. (2011) studied this question.
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