The loss of tolerance to CHI3L1 – A putative role in inflammatory bowel disease?

Publication date: Available online 10 December 2018

Source: Clinical Immunology

Author(s): Claudia Deutschmann, Dirk Roggenbuck, Peter Schierack

Abstract

The incidence of inflammatory bowel disease (IBD) is steadily increasing. IBD is characterized by a chronic inflammation of the gastrointestinal tract and is classified into the two main groups Crohn's disease (CD) and ulcerative colitis (UC). Genetic predispositions, environmental factors and a dysregulated immune response are known to part take in the onset of IBD. However, their etiopathogenesis is still not fully understood. In the last decade, there is growing evidence of the involvement of the 18- glycosylhydrolase family member Chitinase-3-like protein 1 (CHI3L1) in IBD. CHI3L1 is associated with various diseases including cancer and chronic inflammatory conditions like rheumatoid arthritis, IBD and even neurological disorders where it can act as a chemotractant, mitogen or growth factor. In this review will focus on the role of autoimmunity to CHI3L1 in IBD in the context of its expression in inflamed colonic epithelia and interaction with intestinal microbiota. It will further provide insight into the interaction of CHI3L1 with different mechanisms of the innate and adaptive immune response in IBD.

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