Journal
MUCOSAL IMMUNOLOGY
Volume 6, Issue 4, Pages 751-761Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2012.113
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Funding
- Broad Medical Research Program of the Broad Foundation, USA
- Medical Research Council Trust, UK
- St Mark's Hospital Foundation, UK
- Biotechnology and Biological Research Council Institute Strategic Program for Gut Health and Food Safety [BB/J004529/1]
- Brigid Balfour Fund
- Diabetes UK
- BRC at the Imperial College Healthcare Trust
- Biotechnology and Biological Sciences Research Council [BBS/E/F/00044446] Funding Source: researchfish
- BBSRC [BBS/E/F/00044446] Funding Source: UKRI
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Dendritic cells (DC) migrate to lymph nodes on expression of C-C motif chemokine receptor 7 (CCR7) and control immune activity. Leptin, an immunomodulatory adipokine, functions via leptin receptors, signaling via the long isoform of receptor, LepRb. Leptin promotes DC maturation and increases CCR7 expression on blood DC. Increased mesenteric fat and leptin occur early in Crohn's disease (CD), suggesting leptin-mediated change in intestinal CCR7 expression on DC as a pro-inflammatory mechanism. We have demonstrated CCR7 expression and capacity to migrate to its ligand macrophage inflammatory protein 3 beta in normal human ileal DC but not colonic or blood DC. In CD, functional CCR7 was expressed on DC from all sites. Only DC populations containing CCR7-expressing cells produced LepRb; in vitro exposure to leptin also increased expression of functional CCR7 in intestinal DC in a dose-dependent manner. In conclusion, leptin may regulate DC migration from gut, in homeostatic and inflammatory conditions, providing a link between mesenteric obesity and inflammation.
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