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Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine
Published on: May 21, 2012
IL-10-dependent partial refractoriness to Toll-like receptor stimulation modulates gut mucosal dendritic cell
Ivan Monteleone1, Andrew M Platt, Elin Jaensson
1Division of Immunology Infection and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Glasgow, Scotland, UK.
European Journal of Immunology
|May 8, 2008
Summary
Intestinal dendritic cells (DCs) express Toll-like receptors (TLRs) but produce IL-10, maintaining immune tolerance. This IL-10 production keeps gut DCs unresponsive to TLRs, crucial for immune homeostasis.
Area of Science:
- Immunology
- Gastroenterology
- Cell Biology
Background:
- The intestinal immune system typically induces tolerance to antigens, contrasting with constant exposure to pattern recognition receptor ligands.
- Dendritic cells (DCs) in the lamina propria (LP) of the mouse intestine may possess inherent tolerogenic properties.
- The role of Toll-like receptors (TLRs) in the function of intestinal DCs requires further investigation.
Purpose of the Study:
- To explore the relationship between TLR expression and the tolerogenic function of intestinal lamina propria dendritic cells (LP DCs).
- To investigate the impact of TLR ligation on LP DC function, including cytokine production and co-stimulatory molecule expression.
Main Methods:
- Compared TLR protein expression levels in LP DCs versus spleen and mesenteric lymph node (MLN) DCs.
- Analyzed TLR expression patterns along the length of the small intestine and colon.
- Assessed the expression of co-stimulatory molecules (CD40, CD80, CD86) and CCR7 on LP DCs.
- Investigated the induction of IL-12 and IL-10 production by LP DCs upon TLR stimulation, with and without IL-10 blockade.
Main Results:
- LP DCs exhibited higher expression of TLR 2, 3, 4, and 9 compared to spleen and MLN DCs.
- Most TLR-expressing LP DCs were characterized as CD11c(lo), class II MHC(lo), CD103(-), CD11b(-), and F4/80(-).
- TLR expression was lower in the upper small intestine and higher in the distal small intestine and colon.
- TLR stimulation upregulated co-stimulatory molecules on CD11c(lo) LP DCs but induced minimal IL-12.
- Constitutive IL-10 production by LP DCs was observed, which suppressed IL-12 induction and was reversible by IL-10 blockade.
Conclusions:
- Interleukin-10 (IL-10) production by intestinal lamina propria dendritic cells (LP DCs) plays a critical role in maintaining a partially unresponsive state to Toll-like receptor (TLR) ligation.
- This IL-10-mediated suppression is essential for immune homeostasis in the gut, contributing to the induction of immunological tolerance.
- Intestinal DCs, through their unique response to TLRs modulated by IL-10, are key players in balancing immune activation and tolerance in the intestinal environment.
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