PMID- 16785517
OWN - NLM
STAT- MEDLINE
DCOM- 20060809
LR  - 20190516
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 177
IP  - 1
DP  - 2006 Jul 1
TI  - Galectin-1-matured human monocyte-derived dendritic cells have enhanced migration 
      through extracellular matrix.
PG  - 216-26
AB  - Dendritic cells (DCs) are potent mediators of the immune response, and can be 
      activated by exogenous pathogen components. Galectin-1 is a member of the 
      conserved beta-galactoside-binding lectin family that binds galactoside residues 
      on cell surface glycoconjugates. Galectin-1 is known to play a role in immune 
      regulation via action on multiple immune cells. However, its effects on human DCs 
      are unknown. In this study, we show that galectin-1 induces a phenotypic and 
      functional maturation in human monocyte-derived DCs (MDDCs) similar to but 
      distinct from the activity of the exogenous pathogen stimuli, LPS. Immature human 
      MDDCs exposed to galectin-1 up-regulated cell surface markers characteristic of 
      DC maturation (CD40, CD83, CD86, and HLA-DR), secreted high levels of IL-6 and 
      TNF-alpha, stimulated T cell proliferation, and showed reduced endocytic 
      capacity, similar to LPS-matured MDDCs. However, unlike LPS-matured DCs, 
      galectin-1-treated MDDCs did not produce the Th1-polarizing cytokine IL-12. 
      Microarray analysis revealed that in addition to modulating many of the same DC 
      maturation genes as LPS, galectin-1 also uniquely up-regulated a significant 
      subset of genes related to cell migration through the extracellular matrix (ECM). 
      Indeed, compared with LPS, galectin-1-treated human MDDCs exhibited significantly 
      better chemotactic migration through Matrigel, an in vitro ECM model. Our 
      findings show that galectin-1 is a novel endogenous activator of human MDDCs that 
      up-regulates a significant subset of genes distinct from those regulated by a 
      model exogenous stimulus (LPS). One unique effect of galectin-1 is to increase DC 
      migration through the ECM, suggesting that galectin-1 may be an important 
      component in initiating an immune response.
FAU - Fulcher, Jennifer A
AU  - Fulcher JA
AD  - Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, 
      University of California-Los Angeles, Los Angeles, CA 90095, USA.
FAU - Hashimi, Sara T
AU  - Hashimi ST
FAU - Levroney, Ernest L
AU  - Levroney EL
FAU - Pang, Mabel
AU  - Pang M
FAU - Gurney, Kevin B
AU  - Gurney KB
FAU - Baum, Linda G
AU  - Baum LG
FAU - Lee, Benhur
AU  - Lee B
LA  - eng
GR  - AI 06094/AI/NIAID NIH HHS/United States
GR  - AI 07126-30/AI/NIAID NIH HHS/United States
GR  - AI 61824/AI/NIAID NIH HHS/United States
GR  - CA 16042/CA/NCI NIH HHS/United States
GR  - GM 08042/GM/NIGMS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Cytokines)
RN  - 0 (Galectin 1)
RN  - 0 (Glycoconjugates)
RN  - 0 (Immunoconjugates)
RN  - 0 (Lipopolysaccharides)
SB  - IM
MH  - Cell Differentiation/genetics/*immunology
MH  - Cell Membrane/immunology/metabolism
MH  - Cell Movement/genetics/*immunology
MH  - Cells, Cultured
MH  - Coculture Techniques
MH  - Cytokines/metabolism
MH  - Dendritic Cells/*cytology/immunology/*metabolism
MH  - Extracellular Matrix/*immunology/*metabolism
MH  - Galectin 1/metabolism/*physiology
MH  - Gene Expression Regulation/immunology
MH  - Glycoconjugates/metabolism
MH  - Humans
MH  - Immunoconjugates/metabolism
MH  - Immunophenotyping
MH  - Lipopolysaccharides/pharmacology
MH  - Monocytes/*cytology/immunology/metabolism
MH  - Protein Binding/immunology
MH  - T-Lymphocyte Subsets/cytology/immunology/metabolism
MH  - Up-Regulation/genetics/immunology
EDAT- 2006/06/21 09:00
MHDA- 2006/08/10 09:00
CRDT- 2006/06/21 09:00
PHST- 2006/06/21 09:00 [pubmed]
PHST- 2006/08/10 09:00 [medline]
PHST- 2006/06/21 09:00 [entrez]
AID - 177/1/216 [pii]
AID - 10.4049/jimmunol.177.1.216 [doi]
PST - ppublish
SO  - J Immunol. 2006 Jul 1;177(1):216-26. doi: 10.4049/jimmunol.177.1.216.