Study of tumor necrosis factor receptor in the inflammatory bowel disease

Ulcerative colitis (UC) and Crohn's disease (CD) are part of Inflammatory Bowel Diseases (IBD) and have pathophysiological processes such as bowel necrosis and enteric neurons and enteric glial cells. In addition, the main inflammatory mediator is related to the tumor necrosis factor-alpha (TNF-alpha). TNF-alpha is a mediator of the intestinal inflammatory processes, thus being one of the main cytokines involved in the pathogenesis of IBD, however, its levels, when measured, are present in the serum of patients with IBD. In addition, TNF-alpha plays an important role in promoting inflammation, such as the production of interleukins (IL), for instance IL-1 beta and IL-6. There are two receptors for TNF as following: The tumor necrosis factor 1 receptor (TNFR1); and the tumor necrosis factor 2 receptor (TNFR2). They are involved in the pathogenesis of IBD and their receptors have been detected in IBD and their expression is correlated with disease activity. The soluble TNF form binds to the TNFR1 receptor with, and its activation results in a signaling cascade effects such as apoptosis, cell proliferation and cytokine secretion. In contrast, the transmembrane TNF form can bind both to TNFR1 and TNFR2. Recent studies have suggested that TNF-alpha is one of the main pro-inflammatory cytokines involved in the pathogenesis of IBD, since TNF levels are present in the serum of both patients with UC and CD. Intravenous and subcutaneous biologics targeting TNF-alpha have revolutionized the treatment of IBD, thus becoming the best available agents to induce and maintain IBD remission. The application of antibodies aimed at neutralizing TNF- a in patients with IBD that induce a satisfactory clinical response in up to 60% of patients, and also induced long-term maintenance of disease remission in most patients. It has been suggested that anti-TNF-alpha agents inactivate the pro-inflammatory cytokine TNF-alpha by direct neutralization, i. e., resulting in suppression of inflammation. However, anti-TNF-alpha antibodies perform more complex functions than a simple blockade.

Automated summary

Ulcerative colitis (UC) and Crohn's disease (CD) are types of Inflammatory Bowel Diseases (IBD) characterized by bowel necrosis and the involvement of enteric neurons and glial cells. The main inflammatory mediator is tumor necrosis factor-alpha (TNF-alpha), which is also associated with the production of other cytokines like interleukins (IL). TNF-alpha acts through two receptors, TNFR1 and TNFR2, which have been detected in IBD and their expression correlates with disease activity. Biologic agents targeting TNF-alpha have revolutionized IBD treatment by inducing and maintaining disease remission in a majority of patients.