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Details for phenotype: regulation of innate immune response

EndoNet ID: ENP00369

Name

regulation of innate immune response

General information

This phenotype is not pathologic

Links to other resources

GO
MeSH term 68007113

Phenotype triggers

  • normal activity of Probable G-protein coupled receptor 132
    in macrophage
    • 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
    in dendritic_cell_in_lymphoid_tissues
    • 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
    in lipocyte_of_liver
    • 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
    in lipocyte_of_liver
    • 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
    in lipocyte_of_liver
    • 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