Inflammatory bowel disease (IBD) is produced by an exaggerated response to bacterial flora within the intestinal mucous, in which both environmental and genetic factors are involved. T lymphocytes are involved during the genesis and maintenance of IBD, and their cytokine profile in Crohn's disease (mostly Th1 cytokines) is different from that in ulcerative colitis (mainly Th2 cytokines). After the inflammatory response has been established, the balance between proinflammatory and regulatory cytokines determines the degree of mucosal damage and the form of presentation. A deeper knowledge of the immunological mechanisms involved in IBD has opened new research lines aimed to the development of new therapies such as the neutralization of proinflammatory cytokines with antibodies and the administration of antiinflammatory cytokines, which are currently at different stages of research.