Abstract
Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is a complex immune-mediated disease of the gastrointestinal tract that increases morbidity and negatively influences the quality of life. Intestinal mononuclear phagocytes (MNPs) have a crucial role in maintaining epithelial barrier integrity while controlling pathogen invasion by activating an appropriate immune response. However, in genetically predisposed individuals, uncontrolled immune activation to intestinal flora is thought to underlie the chronic mucosal inflammation that can ultimately result in IBD. Thus, MNPs are involved in fine-tuning mucosal immune system responsiveness and have a critical role in maintaining homeostasis or, potentially, the emergence of IBD. MNPs include monocytes, macrophages and dendritic cells, which are functionally diverse but highly complementary. Despite their crucial role in maintaining intestinal homeostasis, specific functions of human MNP subsets are poorly understood, especially during diseases such as IBD. Here we review the current understanding of MNP ontogeny, as well as the recently identified human intestinal MNP subsets, and discuss their role in health and IBD.
Highlights
Crohn’s disease and ulcerative colitis (UC) are chronic inflammatory disorders of the digestive tract that comprise the term inflammatory bowel disease (IBD) [1, 2]
IBD is characterized by intestinal microbiota dysbiosis, with a reduction in both bacterial quantity and diversity [10, 12, 13]
This review focuses on the current understanding of mononuclear phagocytes (MNPs) subset ontogeny as well as their role in the human intestine during health and IBD
Summary
Crohn’s disease and ulcerative colitis (UC) are chronic inflammatory disorders of the digestive tract that comprise the term inflammatory bowel disease (IBD) [1, 2]. It has recently been shown that the traditional gating strategy characterizing human pDCs, which is CD123+ cells among CD14−CD11c− MNPs, includes pre-cDCs [91, 103] Additional markers such as CD45RA, CX3CR1, and CD33 are required to analyze bona fide pDCs [103] (Figure 1). TREM-1 activation leads to the secretion of pro-inflammatory cytokines and chemokines such as TNF, IL-6, IL-1β, IL-8 and CCL2, and synergizes with TLR activation [251,252,253,254] Our group and another showed that intestinal mature Mfs expressed less TREM-1 than immature Mfs and blood monocytes [253, 255], which has been corroborated by a recent study using scRNA-Seq [
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