Our immunological and molecular knowledge base¹ in idiopathic chronic inflammatory bowel disease (IBD) has seen a tremendous increase over the past few years. Laboratory application of sophisticated new methodologies has revealed a plethora of agonistic and antagonistic factors involved in the pathogenesis of both ulcerative colitis and Crohn’s disease. Proinflammatory and Th2 derived anti-inflammatory cytokines are secreted by and act on various different cell types by forming a complex network of interdigitating molecular pathways with profound effects on epithelial cells, lymphocytes, endothelial cells, and monocytes. This multilayered interplay of humoral factors and various cells at different stages of differentiation appears similar to a symphony where the end result is perfect yet the role of various single instruments remains obscure to the casual listener.

Some of the …