PMID- 16140380
OWN - NLM
STAT- MEDLINE
DCOM- 20060425
LR  - 20141120
IS  - 0161-5890 (Print)
IS  - 0161-5890 (Linking)
VI  - 43
IP  - 9
DP  - 2006 Mar
TI  - Chemotaxis of human monocyte-derived dendritic cells to complement component C1q 
      is mediated by the receptors gC1qR and cC1qR.
PG  - 1402-7
AB  - Dendritic cells (DCs) are recruited to inflammatory sites where they phagocytose 
      and process antigens for subsequent presentation to the T lymphocytes in the 
      lymphoid tissue. Several leukocyte chemoattractants and their specific receptors 
      have been shown to induce the migration of DC. The complement protein C1q has 
      multiple immune functions including acting as a chemoattractant for neutrophils, 
      eosinophils and mast cells. Therefore, the objective of this study was to 
      determine if soluble C1q can induce chemotaxis of DC. Culturing cells in GM-CSF 
      and IL-4 for 5 to 7 days generated human monocyte-derived DCs. In addition, LPS 
      was added from day 5 to 7 to induce DC maturation. Cells were classified as 
      either immature or mature DC by assessing the cell surface markers by flow 
      cytometry, phagocytosis of dextran-FITC and T cell proliferation in an allogenic 
      MLR. Immature DCs express the C1q receptors (C1qR), gC1qR and cC1qR/CR and, 
      accordingly, display a vigorous migratory response to soluble C1q with maximal 
      cell movement observed at 10-50nM. In contrast, mature DCs neither express C1qR 
      nor do move to a gradient of soluble C1q. Varying the concentration gradient of 
      C1q (checkerboard assay) showed that the protein largely induces a chemotactic 
      response. Finally, blocking gC1qR and cC1qR/CR by using specific antibodies 
      abolished the chemotactic response to C1q but had no effect on a different 
      chemoattractant C5a. These results clearly demonstrate that C1q functions as a 
      chemotactic factor for immature DC, and migration is mediated through ligation of 
      both gC1qR and cC1qR/CR.
FAU - Vegh, Zsuzsa
AU  - Vegh Z
AD  - Department of Medicine, Stony Brook University School of Medicine, Stony Brook, 
      NY 11794-8161, USA.
FAU - Kew, Richard R
AU  - Kew RR
FAU - Gruber, Barry L
AU  - Gruber BL
FAU - Ghebrehiwet, Berhane
AU  - Ghebrehiwet B
LA  - eng
GR  - GM 63769/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20050902
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (Antibodies)
RN  - 0 (C1QBP protein, human)
RN  - 0 (Calreticulin)
RN  - 0 (Carrier Proteins)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Mitochondrial Proteins)
RN  - 0 (Receptors, Complement)
RN  - 0 (complement 1q receptor)
RN  - 80295-33-6 (Complement C1q)
SB  - IM
MH  - Animals
MH  - Antibodies/pharmacology
MH  - Calreticulin/antagonists & inhibitors/*metabolism
MH  - Carrier Proteins/antagonists & inhibitors/*metabolism
MH  - Cell Differentiation
MH  - Cell Membrane/immunology
MH  - Chemotactic Factors/metabolism/pharmacology
MH  - Chemotaxis/drug effects/*immunology
MH  - Complement C1q/*metabolism/pharmacology
MH  - Dendritic Cells/cytology/drug effects/*immunology
MH  - Humans
MH  - In Vitro Techniques
MH  - Membrane Glycoproteins/antagonists & inhibitors/*metabolism
MH  - Mitochondrial Proteins/antagonists & inhibitors/*metabolism
MH  - Monocytes/cytology/immunology
MH  - Phenotype
MH  - Rabbits
MH  - Receptors, Complement/antagonists & inhibitors/*metabolism
EDAT- 2005/09/06 09:00
MHDA- 2006/04/28 09:00
CRDT- 2005/09/06 09:00
PHST- 2005/07/07 00:00 [received]
PHST- 2005/09/06 09:00 [pubmed]
PHST- 2006/04/28 09:00 [medline]
PHST- 2005/09/06 09:00 [entrez]
AID - S0161-5890(05)00310-X [pii]
AID - 10.1016/j.molimm.2005.07.030 [doi]
PST - ppublish
SO  - Mol Immunol. 2006 Mar;43(9):1402-7. doi: 10.1016/j.molimm.2005.07.030. Epub 2005 
      Sep 2.