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J Invest Dermatol. 2009 Mar;129(3):573-83. doi: 10.1038/jid.2008.276. Epub 2008 Oct 9.

Endogenous galectin-3 is localized in membrane lipid rafts and regulates migration of dendritic cells.

Author information

1
Department of Dermatology, University of California Davis School of Medicine, Sacramento, California 95817, USA. dkhsu@ucdavis.edu

Abstract

This study reveals a function of endogenous galectin-3, an animal lectin recognizing beta-galactosides, in regulating dendritic cell motility both in vitro and in vivo, which to our knowledge is unreported. First, galectin-3-deficient (gal3(-/-)) bone marrow-derived dendritic cells exhibited defective chemotaxis compared to gal3(+/+) cells. Second, cutaneous dendritic cells in gal3(-/-) mice displayed reduced migration to draining lymph nodes upon hapten stimulation compared to gal3(+/+) mice. Moreover, gal3(-/-) mice were impaired in the development of contact hypersensitivity relative to gal3(+/+) mice in response to a hapten, a process in which dendritic cell trafficking to lymph nodes is critical. In addition, defective signaling was detected in gal3(-/-) cells upon chemokine receptor activation. By immunofluorescence microscopy, we observed that galectin-3 is localized in membrane ruffles and lamellipodia in stimulated dendritic cells and macrophages. Furthermore, galectin-3 was enriched in lipid raft domains under these conditions. Finally, we determined that ruffles on gal3(-/-) cells contained structures with lower complexity compared to gal3(+/+) cells. In view of the participation of membrane ruffles in signal transduction and cell motility, we conclude that galectin-3 regulates cell migration by functioning at these structures.

PMID:
18843294
PMCID:
PMC2645233
DOI:
10.1038/jid.2008.276
[Indexed for MEDLINE]
Free PMC Article

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