Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
15
pubmed:dateCreated
2009-4-10
pubmed:abstractText
Dendritic cells (DCs) are known to produce C1q, the initiator of the classical complement pathway. We demonstrate that murine DCs deficient in C1q (C1qa(-/-)) are poorer than wild-type (WT) DCs at eliciting the proliferation and Th1 differentiation of antigen-specific T cells. These defects result from decreased production of IL-12p70 by C1qa(-/-) DCs and impaired expression of costimulatory molecules CD80 and CD86 in response to CD40 ligation. The defective production of IL-12p70 and the reduced expression of CD80 and CD86 by C1qa(-/-) DCs were specifically mediated via CD40 ligation, as normal levels of IL-12p70 and CD80/86 were observed after ligation of Toll-like receptors (TLRs) on C1qa(-/-) DCs. CD40 ligation on C1qa(-/-) DCs, but not TLR ligation, results in decreased phosphorylation of p38 and ERK1/2 kinases. A strong colocalization of CD40 and C1q was observed by confocal microscopy upon CD40 ligation (but not TLR ligation) on DCs. Furthermore, human DCs from 2 C1q-deficient patients were found to have impaired IL-12p70 production in response to CD40L stimulation. Our novel data suggest that C1q augments the production of IL-12p70 by mouse and human DCs after CD40 triggering and plays important roles in sustaining the maturation of DCs and guiding the activation of T cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1528-0020
pubmed:author
pubmed:issnType
Electronic
pubmed:day
9
pubmed:volume
113
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3485-93
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:19171874-Animals, pubmed-meshheading:19171874-Antigen Presentation, pubmed-meshheading:19171874-Antigens, CD40, pubmed-meshheading:19171874-Apoptosis, pubmed-meshheading:19171874-Calreticulin, pubmed-meshheading:19171874-Cell Communication, pubmed-meshheading:19171874-Cell Differentiation, pubmed-meshheading:19171874-Cells, Cultured, pubmed-meshheading:19171874-Complement C1q, pubmed-meshheading:19171874-Dendritic Cells, pubmed-meshheading:19171874-Female, pubmed-meshheading:19171874-Humans, pubmed-meshheading:19171874-Interferon-gamma, pubmed-meshheading:19171874-Interleukin-12, pubmed-meshheading:19171874-Lymphocyte Transfusion, pubmed-meshheading:19171874-Male, pubmed-meshheading:19171874-Mice, pubmed-meshheading:19171874-Mice, Mutant Strains, pubmed-meshheading:19171874-Mitogen-Activated Protein Kinase 1, pubmed-meshheading:19171874-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:19171874-Phagocytosis, pubmed-meshheading:19171874-Spleen, pubmed-meshheading:19171874-Th1 Cells, pubmed-meshheading:19171874-Toll-Like Receptors, pubmed-meshheading:19171874-p38 Mitogen-Activated Protein Kinases
pubmed:year
2009
pubmed:articleTitle
C1q enhances IFN-gamma production by antigen-specific T cells via the CD40 costimulatory pathway on dendritic cells.
pubmed:affiliation
Molecular Genetics and Rheumatology Section, Faculty of Medicine, Imperial College London, London, United Kingdom.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't