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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
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Enterocyte dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin expression in inflammatory
Jing-Qing Zeng1, Chun-Di Xu1, Tong Zhou1
1Jing-Qing Zeng, Chun-Di Xu, Tong Zhou, Jing Wu, Kai Lin, Wei Liu, Xin-Qiong Wang, Department of Pediatrics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
World Journal of Gastroenterology
|January 10, 2015
Summary
Dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) expression increases in intestinal epithelial cells during inflammatory bowel disease (IBD), correlating with disease severity. Targeting DC-SIGN may offer a therapeutic strategy for IBD.
Area of Science:
- Immunology
- Gastroenterology
- Cell Biology
Background:
- Inflammatory bowel disease (IBD) involves complex immune dysregulation within the intestinal mucosa.
- Intestinal epithelial cells (IECs) play a critical role in maintaining gut homeostasis and immune responses.
- Dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) is a C-type lectin receptor implicated in immune cell interactions.
Purpose of the Study:
- To investigate the expression and role of DC-SIGN in IECs within the context of IBD.
- To explore the correlation between DC-SIGN expression and disease activity in IBD patients and a mouse model.
- To assess the impact of targeting DC-SIGN on T cell responses in experimental colitis.
Main Methods:
- Immunohistochemistry and flow cytometry were used to assess DC-SIGN expression in IECs from IBD patients and a dextran sodium sulfate (DSS)-induced colitis mouse model.
- Disease activity and histopathology scores were evaluated to correlate DC-SIGN levels with disease severity.
- T cell activation, cytokine production (IL-4, IFN-γ), and proliferation were analyzed in co-culture experiments involving IECs and T cells, with and without anti-P-selectin lectin-EGF domain monoclonal antibody (PsL-EGFmAb) treatment.
Main Results:
- DC-SIGN expression was significantly elevated in IECs of IBD patients (Crohn's disease and ulcerative colitis) and mice with DSS-induced colitis compared to controls.
- DC-SIGN expression strongly correlated with disease severity in both human IBD and the mouse model.
- IECs from colitis models promoted T cell proliferation and IL-4 production, while dendritic cells induced a T-helper-1 phenotype; treatment with PsL-EGFmAb suppressed DC-SIGN expression and modulated T cell differentiation and proliferation.
Conclusions:
- IECs regulate intestinal immune responses in IBD, with DC-SIGN playing a key regulatory role.
- Increased DC-SIGN expression in IECs is associated with IBD pathogenesis and severity.
- Targeting DC-SIGN may represent a potential therapeutic avenue for managing IBD by modulating T cell responses.
Keywords:
Dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrinDendritic cellsImmune compartmentalizationInflammatory bowel diseaseIntestinal epithelial cellsMore Related Videos
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