Abstract
The occurrence of epithelial defects in the gut relevantly contributes to the pathogenesis of inflammatory bowel diseases (IBD), whereby the impairment of intestinal epithelial barrier integrity seems to represent a primary trigger as well as a disease amplifying consequence of the chronic inflammatory process. Besides epithelial cell intrinsic factors, accumulated and overwhelmingly activated immune cells and their secretome have been identified as critical modulators of the pathologically altered intestinal epithelial cell (IEC) function in IBD. In this context, over the last 10 years increasing levels of attention have been paid to the group of innate lymphoid cells (ILCs). This is in particular due to a preferential location of these rather newly described innate immune cells in close proximity to mucosal barriers, their profound capacity to secrete effector cytokines and their numerical and functional alteration under chronic inflammatory conditions. Aiming on a comprehensive and updated summary of our current understanding of the bidirectional mucosal crosstalk between ILCs and IECs, this review article will in particular focus on the potential capacity of gut infiltrating type-1, type-2, and type-3 helper ILCs (ILC1s, ILC2s, and ILC3s, respectively) to impact on the survival, differentiation, and barrier function of IECs. Based on data acquired in IBD patients or in experimental models of colitis, we will discuss whether the different ILC subgroups could serve as potential therapeutic targets for maintenance of epithelial integrity and/or mucosal healing in IBD.
Highlights
Worldwide, approximately seven million patients are diagnosed with inflammatory bowel diseases (IBD) [1], a chronically remitting inflammatory disease of the gastrointestinal tract
Still approximately 40% of IBD patients do not show a satisfactory primary response even to these optimized therapeutic regimens or develop a secondary loss of response [5, 9], emphasizing the urgent need to further fine-tune the definition of therapeutic target structures, and/or to better take into account the full spectrum of interacting cellular players involved in the pathogenesis of IBD
It will be of particular importance to better elucidate the complex crosstalk between intestinal epithelial cells (IECs) and subepithelial innate immune cells, which together form an early and tightly regulated line of host defense against invading luminal pathogens
Summary
Besides epithelial cell intrinsic factors, accumulated and overwhelmingly activated immune cells and their secretome have been identified as critical modulators of the pathologically altered intestinal epithelial cell (IEC) function in IBD. In this context, over the last 10 years increasing levels of attention have been paid to the group of innate lymphoid cells (ILCs). Over the last 10 years increasing levels of attention have been paid to the group of innate lymphoid cells (ILCs) This is in particular due to a preferential location of these rather newly described innate immune cells in close proximity to mucosal barriers, their profound capacity to secrete effector cytokines and their numerical and functional alteration under chronic inflammatory conditions.
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