Please use this identifier to cite or link to this item: http://buratest.brunel.ac.uk/handle/2438/14630
Title: A mechanistic role for leptin in human dendritic cell migration: differences between ileum and colon in health and Crohn's disease
Authors: Al-Hassi, HO
Bernardo, D
Murugananthan, AU
Mann, ER
English, NR
Jones, A
Kamm, MA
Arebi, N
Hart, AL
Blakemore, AIF
Stagg, AJ
Knight, SC
Keywords: Science & Technology;Life Sciences & Biomedicine;Immunology;IMMUNOLOGY;INFLAMMATORY-BOWEL-DISEASE;CHEMOKINE RECEPTOR CCR7;MESENTERIC LYMPH-NODES;INTESTINAL INFLAMMATION;STIMULATORY CAPACITY;CYTOKINE PRODUCTION;SIGNALING PATHWAY;ADIPOSE-TISSUE;IN-VITRO;MATURATION
Issue Date: 2013
Publisher: NATURE PUBLISHING GROUP
Citation: MUCOSAL IMMUNOLOGY, 2013, 6 (4), pp. 751 - 761 (11)
Abstract: 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 3β 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.
URI: http://bura.brunel.ac.uk/handle/2438/14630
DOI: http://dx.doi.org/10.1038/mi.2012.113
ISSN: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000322535800009&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=f12c8c83318cf2733e615e54d9ed7ad5
http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000322535800009&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=f12c8c83318cf2733e615e54d9ed7ad5
1933-0219
Appears in Collections:Dept of Life Sciences Research Papers



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