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Statistic
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Details for phenotype: regulation of innate immune response
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EndoNet ID: ENP00369
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Name
regulation of innate immune response
General information
This phenotype is not pathologic
Links to other resources
GO
regulation of innate immune response
MeSH term
68007113
Phenotype triggers
normal activity of
Probable G-protein coupled receptor 132
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in
macrophage
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Innate immune responses of macrophages may be regulated via G2A in response to local fluctuations in lysolipids encountered during infection and inflammation. It is possible that LPC produced at sites of inflammation and from disintegrating apoptotic/necrotic cell membranes may be a novel “molecular pattern” recognized by G2A to modulate innate immune processes and the initiation and/or resolution of inflammatory responses.
[1]
normal activity of
Probable G-protein coupled receptor 132
ui-button
in
dendritic_cell_in_lymphoid_tissues
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Innate immune responses of dendritic cells may be regulated via G2A in response to local fluctuations in lysolipids encountered during infection and inflammation. It is possible that LPC produced at sites of inflammation and from disintegrating apoptotic/necrotic cell membranes may be a novel “molecular pattern” recognized by G2A to modulate innate immune processes and the initiation and/or resolution of inflammatory responses.
[1]
normal activity of
TLR4
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in
lipocyte_of_liver
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TLR4-stimulated HSCs produce various chemokines and express adhesion molecules to recruit Kupffer cells and/or circulating macrophages by the site of HSCs.
[2]
The activation of TLR4 signaling enhances TGF-β signaling, that downregulates the expression of BMP and activin membrane bound inhibitor (Bambi) for firogenic response.
[3]
normal activity of
CD14
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in
lipocyte_of_liver
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Activated human HSCs express TLR4 and its coreceptor CD14.TLR4 signaling in HSCs enhances the recruitment of inflammatory cells and downregulates BMP and activin membrane bound inhibitor (Bambi) for fibrogenic response.
[3]
more activity (high ligand concentration, overexpression) of
TLR2
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in
lipocyte_of_liver
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Upregulated TLR2 expression primes HSCs to increase NF-kappa B activation and IL-8 production in response to TLR2 ligands. This is important for the induction of potent innate immune response.
[4]
HSCs barely respond to TLR2 ligands. Initiation by inflammatory mediators such as TNF-α, IL-1β, and LPS might be required for fulfilling TLR2 signaling in HSCs.
[3]
Reference