Tsvetelina Velikova

By Tsvetelina Velikova, Dobroslav Kyurkchiev, Ekaterina Ivanova- Todorova, Zoya Spassova, Spaska Stanilova and Iskra Altankova

Cells of the innate and the adaptive immune system have been identified as the key players in inflammatory bowel disease (IBD) pathogenesis, and the cytokines are central components of the inflammatory pathways that take place in the gut mucosa during the active and chronic phases of IBD. The effector cell response is largely determined by the type of cytokines that predominate in the intestinal mucosa. Here we describe the main cytokine players in intestinal inflammation during IBD—related to innate immune responses (tumor necrosis factor α—TNFα), TNF-like cytokine 1A, IL-8), and related to adaptive immune responses—Th1 (IL-1β, IL-18, IFNγ, IL-12), Th2 (IL-4, IL-5, IL-13, IL-11, IL-33), Th17 (IL-17A, IL-17F, IL-21, IL-22, IL-25, IL-27), cytokines required for Th17 development (IL-6, TGFβ, IL-23), anti-inflammatory cytokine IL-10 and Tregs along with IL-2. Recently described innate lymphoid cells (ILCs) could also be potential sources of IFN-γ, TNF, IL-5, IL-13, IL-17, and IL-22. The effects of cytokines in the gut are described in conjunction with the clinical implication and available biologic therapy. The data in the literature and our own results make us believe that in order to achieve immune homeostasis in the gut, pro-inflammatory and anti-inflammatory responses that define the mucosal cell immunophenotype should achieve balance.

Part of the book: New Insights into Inflammatory Bowel Disease