Ulcerative colitis (UC) is a relapsing inflammatory bowel disease whose pathogenesis has yet to be defined completely. A genetic predisposition is needed to develop the colitis, but environmental factors are necessary to trigger an exaggerated and aberrant immune response, which stands at the basis of the mucosal healing. Cytokines, small cell-signaling protein molecules secreted by various types of cells including immune and glia cells, are the main mediators of the mucosal healing in IBD; ulcerative colitis is characterized by a Th2 atypical immune response, since, beside the classical proinflammatory cytokines, such as IL-1, IL-6, and TNF-α, in the pathogenesis of UC, we find a complex network in which the Th2 cytokines, IL-10 and IL-13, play a key role, but little IL-4 was found. Our aim was to review the literature to point out the state of the art in terms of cytokines because the knowledge of cytokine network in UC could lead to the discovery of new therapeutical targets. 1. Introduction Ulcerative colitis (UC), a form of disease belonging to the so-called inflammatory bowel diseases (IBDs), is characterized by continuous inflammation of the intestinal lamina propria, starting from the rectum and potentially involving the whole colonic mucosa. The course of UC is typically unpredictable; it is a chronic disease characterized by spontaneous remittances and relapses [1]. At present, its pathogenesis is still unclear, but evidence suggests that the disease occurs in genetically susceptible subjects, and it is trigged by environmental factors, which lead to an exaggerated and uncontrolled immune response [2–9]. However, genetic susceptibility itself is not sufficient to explain the development of IBD; in fact, environmental triggers have been identified as agents able to disrupt or at least to affect the mucosal barrier, such as NSAIDs, antibiotics, and viral and bacterial infections [10]. Actually, disease expression seems to be the consequence of a dysregulated immune response to both bacteria and bacterial products in a susceptible host; in fact, while inflammatory response against luminal antigens is suppressed in healthy individuals, a destructive immune response is initiated in IBD patients. In this context, the immune response plays a key role in the initiation, augmentation, and perpetuation of the disease. In IBD, in fact, there is a loss of immune tolerance towards the luminal antigens and the commensal flora. This aberrant immune response is mediated by different cytokines, small cell-signaling protein molecules secreted by various types
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