T-helper cell subsets, key cytokines and chemokines in the pathogenesis of inflammatory bowel disease (Part 2)*

Abstract

Studies in recent decades have identified the role of various T-helper cell subsets in the pathogenesis of inflammatory bowel diseases (IBD) and have shown the importance of cytokine-mediated regulation of the immune response in patients with ulcerative colitis (UC) and Crohn’s disease (CD). The imbalance between pro-inflammatory and anti-inflammatory cytokines in IBD prevents resolution of inflammation and leads to chronic course, disease progression and tissue destruction. In the review article, the role of key cytokines that are important in the development and progression of IBD is discussed. Of the pro-inflammatory mediators involved in the pathogenesis of IBD, special attention is currently paid to chemokines – cytokines belonging to chemoattractants. Chemokines are responsible for directed migration and attraction of cells expressing a certain set of receptors to organs, tissues and foci of inflammation. The article provides unique data on the importance of some chemokines in IBD. Cytokines, chemokines and their receptors are considered as potential therapeutic targets in IBD. Cytokine-targeted therapy using antibodies against TNF-α and antibodies to IL-12/IL-23 have already shown high efficiency and safety in randomized clinical trials, as well as in real clinical practice in patients with IBD. The data presented by the authors are important for clarifying the role of immunological processes, including microbiome-dependent ones, in the etiopathogenesis of IBD. Key words: inflammatory bowel disease, ulcerative colitis, Crohn’s disease, T-helper cell subsets, cytokines, chemokines, gut microbiome