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Galectin-3 modulates Th17 responses by regulating dendritic cell cytokines.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Fermin Lee, Agnes Chen, Huan-Yuan Wan, Lei Wu, Sheng-Yang Yu, Jhang-Sian Huang, Annie C. Miaw, Shi-Chuen Hsu, Daniel K. Wu-Hsieh, Betty A. Liu, Fu-Tong
Description	Author Affiliation: Fermin Lee A ( Department of Dermatology, University of California, Davis, School of Medicine, Sacramento, California.)
Abstract	Galectin-3 is a ß-galactoside-binding animal lectin with diverse functions, including regulation of T helper (Th) 1 and Th2 responses. Current data indicate that galectin-3 expressed in dendritic cells (DCs) may be contributory. Th17 cells have emerged as critical inducers of tissue inflammation in autoimmune disease and important mediators of host defense against fungal pathogens, although little is known about galectin-3 involvement in Th17 development. We investigated the role of galectin-3 in the induction of Th17 immunity in galectin-3-deficient (gal3(-/-)) and gal3(+/+) mouse bone marrow-derived DCs. We demonstrate that intracellular galectin-3 negatively regulates Th17 polarization in response to the dectin-1 agonist curdlan (a ß-glucan present on the cell wall of fungal species) and lipopolysaccharide, agents that prime DCs for Th17 differentiation. On activation of dectin-1, gal3(-/-) DCs secreted higher levels of the Th17-axis cytokine IL-23 compared with gal3(+/+) DCs and contained higher levels of activated c-Rel, an NF-κB subunit that promotes IL-23 expression. Levels of active Raf-1, a kinase that participates in downstream inhibition of c-Rel binding to the IL23A promoter, were impaired in gal3(-/-) DCs. Modulation of Th17 by galectin-3 in DCs also occurred in vivo because adoptive transfer of gal3(-/-) DCs exposed to Candida albicans conferred higher Th17 responses and protection against fungal infection. We conclude that galectin-3 suppresses Th17 responses by regulating DC cytokine production.
File Format	HTM / HTML
ISSN	00029440
e-ISSN	15252191
DOI	10.1016/j.ajpath.2013.06.017
Journal	The American Journal of Pathology
Issue Number	4
Volume Number	183
Language	English
Publisher	Elsevier (on behalf of the American Society for Investigative Pathology)
Publisher Date	2013-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Research Support, N.i.h., Extramural Cell Polarity Candidiasis Dendritic Cells Microbiology Interleukin-23 Biosynthesis Adoptive Transfer Beta-glucans Immunity Lipopolysaccharides Immunology Extracellular Signal-regulated Map Kinases Physiology Cytokines Signal Transduction Deficiency Mice, Inbred C57bl Discipline Pathology Pharmacology Metabolism Drug Effects Pathology Proto-oncogene Proteins C-rel Animals Proto-oncogene Proteins C-raf Lectins, C-type Models, Biological Galectin 3 Agonists Th17 Cells Mice Enzyme Activation Enzymology Candida Albicans
Content Type	Text
Resource Type	Article
Subject	Pathology and Forensic Medicine

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