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CXCR4 — IRF6
Text-mined interactions from Literome
Juffermans et al., J Infect Dis 2000
:
Thalidomide produced a dose dependent inhibition of
lipopolysaccharide (LPS) induced
up-regulation of
CXCR4 and CCR5 in vitro
Juffermans et al., J Infect Dis 2002
(Endotoxemia...) :
To test the hypothesis that an
LPS effect on
CXC chemokine receptor 4 (CXCR4) and CC chemokine receptor 5 (CCR5), known coreceptors for HIV, contributes to this effect, 8 healthy men were intravenously injected with Escherichia coli LPS ( 4 ng/kg ), and monocyte CXCR4 and CCR5 expression was monitored by fluorescence activated cell sorter analysis ... In whole blood in vitro, not only
LPS but also lipoarabinomannan ( a cell wall component of Mycobacterium tuberculosis ) and lipoteichoic acid ( a cell wall component of Staphylococcus aureus )
down-regulated the expression of
CXCR4 and CCR5 on monocytes ( all P < .05 )
Cruz et al., Arch Dermatol Res 2005
(Dermatitis, Allergic Contact) :
Lipopolysaccharide (LPS) , which induces the maturation of DC, also
reduced surface CCR6 and
CXCR4 expression
Li et al., Blood 2007
(MAP Kinase Signaling System) :
Specific inhibition of ERK during CB DC maturation enhanced
LPS induced
up-regulation of CCR7 and
CXCR4 on CB DCs and their chemotaxis toward CCL19 and CXCL12, to a level similar to that of mature AB DCs ... Overall, monocyte derived CB DCs responded to LPS with stronger and sustained ERK activation, which negatively correlated with
LPS induced
up-regulation of CCR7 and
CXCR4 on CB DCs and their migratory responses
Kim et al., Int J Hematol 2007
:
We show that
LPS reduces
CXCR4 surface expression in a dose- and time dependent manner in neutrophils and monocytes, but not in lymphocytes
Gong et al., J Endod 2010
(Inflammation) :
All concentrations of LPS inhibited SDF-1alpha production except that 1 microg/mL
LPS increased the expression of
CXCR4
Cheng et al., Zhongguo Shi Yan Xue Ye Xue Za Zhi 2011
:
Further study found that
LPS did not
affect the expression level of
CXCR4 on CD34 ( + ) cells, but could inhibit the spontaneous migration ability of CD34 ( + ) cells