Abstract
Background Intestinal monocytes/macrophages sustain the intestinal immune homeostasis and might be an attractive therapeutic target for the management of inflammatory bowel disease (IBD). Granulocyte macrophage colony-stimulating factor (GM-CSF) exerts beneficial effects on intestinal inflammation and promotes signal transducer and activator of transcription 3 (STAT3)-mediated expansion of myeloid-derived suppressor cells (MDSCs). However, the full action mechanism of GM-CSF, and especially whether monocytes mediate its therapeutic effects in vivo, had not been previously elucidated. Conclusions This review article summarizes recent developments in the immunology of mucosal diseases and describes new aspects of the role of myeloid regulatory cells in IBD and the function of GM-CSF in maintaining the intestinal immune homeostasis in Crohn’s disease (CD). This review article highlights the exploration of stimulating in addition to suppressive therapies for patients with IBD and underpins that myeloid regulatory cells might become a promising novel cell-based therapeutic option.
Highlights
Crohn’s disease (CD) is a chronic relapsing disease and is a manifestation of a dysregulated immune response against the microorganisms of the intestinal flora in genetically susceptible individuals [1]
Various components of the mucosal immune system are implicated in the pathogenesis of inflammatory bowel diseases (IBD) and include intestinal epithelial cells; innate lymphoid cells; cells of the innate immune system such as monocytes, macrophages, neutrophils, and dendritic cells (DCs); the adaptive immune system with T and B cells; and their secretion products (Fig. 1)
Our findings suggest that the early imprinting of monocytes after activation with Granulocyte macrophage colony-stimulating factor (GM-CSF) is of crucial importance, because monocytes play an important role during the recruitment phase of the innate immune response and have the potential to regulate adaptive immune mechanisms
Summary
Crohn’s disease (CD) is a chronic relapsing disease and is a manifestation of a dysregulated immune response against the microorganisms of the intestinal flora in genetically susceptible individuals [1]. Recent work suggests an important protective role of monocytes/macrophages and possible homeostatic mechanisms to restrain acute and chronic intestinal inflammation (reviewed in [3]). We showed that GM-CSF may regulate the homing molecules CCR2 and CCR6 on human monocytes [14], which are involved in regulating several aspects of mucosal immunity, including the ability to mediate the recruitment of innate immune cells to the sites of epithelial inflammation.
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