Abstract
Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract. Though its exact etiology is still unclear, it is proposed that an imbalance in the intestinal homeostasis leads to a disturbed interaction between commensal microbiota and the mucosal immune system. Previous studies have shown that both innate and adaptive immunity are involved in an overwhelming colon inflammation, and thus contribute to the pathogenesis of IBD. In innate immunity, several pattern recognition receptors such as Toll-like receptors, NOD-like receptors or C-type lectin receptors (CLRs) are involved in IBD pathogenesis. Myeloid CLRs are mainly expressed by antigen-presenting cells and bind to glycan structures present on self or foreign antigens. The Macrophage-restricted C-type lectin (MCL) and the Dendritic cell immunoreceptor (DCIR) are two poorly characterized members of the CLR family. In this study, we investigated the role of MCL and DCIR in the pathogenesis of murine colitis. Both CLRs bound to intestinal microbiota to a different extent. They modulated the production of pro-inflammatory cytokines by antigen-presenting cells upon stimulation with heat-killed microbiota and impacted subsequent T cell responses. To analyze whether MCL and DCIR contribute to the pathogenesis of IBD, the dextran sulfate sodium (DSS) murine colitis model was employed. MCL−/− as well as DCIR−/− mice exhibited only a slightly increased severity of disease compared to wild-type mice indicating a limited role for MCL and DCIR in the regulation of intestinal immunity.
Highlights
Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract
Macrophage galactose-type lectin-1 (MGL1)-hFc was used as positive control since binding of this C-type lectin receptors (CLRs) to commensal microbiota was shown in a previous study [20]
IL-10 production did not differ between wild-type and CLR-deficient antigen presenting cells (APCs) (Figure S2). These findings indicate that the recognition of microbiota by Macrophage-restricted C-type lectin (MCL) and Dendritic cell immunoreceptor (DCIR) correlates with a modulated pro-inflammatory cytokine production by APCs
Summary
Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract. There are two major clinical forms: ulcerative colitis (UC) and Crohn’s disease (CD) [1]. UC mainly affects the mucosa of the colon and rectum, whereas inflammation in CD may occur in any part of the gastrointestinal tract [2]. Several factors were reported to play a role in IBD pathogenesis such as environmental factors, diet, genetic factors and the immune system [1]. These factors can influence the composition of commensal microorganisms in the intestine followed by an imbalanced intestinal homeostasis which is a major characteristic feature of IBD [4]
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