Pro-Inflammatory Cytokines in the Pathogenesis of IBD
By W. Strober, I. Fuss. Gastroenterology, 2011
1,051 citations recorded by the source corpus.
The cytokine responses characterizing the inflammatory bowel diseases (IBDs) are the key pathophysiologic elements that govern the initiation, evolution and, ultimately, the resolution of these forms of inflammation. Studies over the last two decades now provide a detailed (but not yet complete) picture of the nature of these responses. The first tier of cytokine responses are governed by the T cell differentiation patterns dominating the disease. Thus, in Crohn’s disease, the major cytokines arise from Th1 and Th17 CD4+ T cell differentiation and consist of IFN-γ and IL-17/IL-22 generated by these types of differentiation. The relative importance of these cytokines to Crohn’s inflammation is still unclear, although evidence is mounting that IFN-γ is primus inter pare (first among equals). In contrast, in ulcerative colitis a Th2-like differentiation process is paramount which results in the expansion of NKT cells producing IL-13 (and perhaps IL-5). These disease-specific cytokine patterns give rise to a second tier of cytokines that span the Th1/Th17–Th2 divide and act as upstream facilitators and downstream mediators of inflammation. These cytokines include the well-known TNF-α, IL-1β, IL-6 triumphirate as well as a more recently studied cytokine known as TL1A. In this review, we will explore this cytokine landscape with the view of providing an understanding of how recent and future anti-cytokine therapies actually function.
Subfields: Genetics, Immunology
View Paper: https://www.semanticscholar.org/paper/05a7b93a1f0ae977cb27930155f6bf2c91576fea
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Citations in the corpus
- A Comprehensive Review and Update on the Pathogenesis of Inflammatory Bowel Disease (2019, background): “IL-13, a key effector Th2 cytokine in ulcerative colitis, also shows the ability to impair epithelial barrier function by affecting epithelial apoptosis, tight junctions, and reconstitution velocity [57].”