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C1QA — TNF
Text-mined interactions from Literome
Lurton et al., Exp Lung Res 1999
:
Regulation of human lung fibroblast
C1q-receptors by transforming growth factor-beta and
tumor necrosis factor-alpha
Bajtay et al., Eur J Immunol 2000
:
Studying the functional consequences of the interaction, we found that the release of
TNF-alpha from Mphi is
induced by
C1q but not by MBL
Csomor et al., Mol Immunol 2007
:
Immobilized
C1q induced maturation of MDCs and enhanced secretion of IL-12 and
TNF-alpha , moreover, elevated their T-cell stimulating capacity
Arora et al., Cytokine 2009
:
In the
presence of
TNF , both mAbs bound
C1q in in vitro assays, but etanercept did not bind C1q under any conditions
Fraser et al., J Neurochem 2010
(Blister) :
Microglia added to C1q coated wells or fed apoptotic neurons or neuronal blebs coated with C1q suppressed the lipopolysaccharide induced production of proinflammatory cytokines interleukin (IL)-1alpha, IL-1beta, IL-6 and
TNF-alpha , while the presence of
C1q enhanced levels of the chemokine MCP-1/CCL2
Leu et al., Immunobiology 1993
:
Inhibitor of C1q secretion suppresses the macrophage response to lipid A for nitric oxide but not for TNF production : evidence for a
role of
C1q in autocrine binding of
TNF ... C1q was confirmed to bind to macrophages at 4 degrees C as detected by FITC anti-C1q, F ( ab ' ) 2 and such
C1q binding
promoted a corresponding increased binding of
PE-TNF ... Since TNF binding to DHP treated macrophages was reconstituted by the binding of exogenous C1q to the cells, it appears that
C1q may be
involved in the modulation of autocrine binding of
TNF for subsequent generation of cytotoxic NO
Jiang et al., Cell Immunol 1996
:
The
role of complement subcomponent
C1q in the modulation of
TNF-alpha binding to L929 cells to mediate cytotoxicity and nitric oxide ( NO ) generation was investigated
Jiang et al., Scand J Immunol 1996
:
In the present study, the putative
role of
C1q in increasing
TNF-alpha binding to L929 cells to mediate cytotoxicity was explored
Bottazzi et al., J Biol Chem 1997
:
The capacity to bind
C1q , mediated by the pentraxin domain, is consistent with the view that PTX3, produced in tissues by endothelial cells or macrophages in
response to interleukin-1 and
tumor necrosis factor , may act as a local regulator of innate immunity