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Details for anatomical structure: monocyte

EndoNet ID: ENC00247

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Synonyms

monocyte, , Monocytus

General information

mononuclear leukocyte; reniform nucleus; contains lysosomes and is highly motile; can pass walls of capillaries and venules to get to inflamed tissues; involved in cellular phagocytosis immune reaction

Links to other resources

Cytomer cy0049449

Larger structures

  • circulatory_system__hematopoietic_system
  • lymph_node
  • immune_system
  • blood
  • bone_marrow

Substructures

    Secreted hormones

    • Hormone: MIG

    • Hormone: ADM

    • Hormone: complement factor B

    • Hormone: alpha-AGP

      • AGP, a highly glycosylated polypeptide chain, is expressed in human liver and in other cells, including human breast epithelial cells, endothelial cells, and cultured human granulocytes and monocytes. [1]

    • Hormone: IL-1 beta

      • IL-1β is abundantly secreted by activated macrophages and blood monocytes. [2]

    • Hormone: oncostatin M

      • OSM is produced by activated monocyte and T-lymphocyte cell lines. [3]

    • Hormone: C-C motif chemokine 2

    • Hormone: ENA-78

    • Hormone: GRObeta

    • Hormone: MCP-2

    • Hormone: MDC

    • Hormone: MIP-1 beta

    • Hormone: M-CSF

    • Hormone: G-CSF

    • Hormone: IL-1 alpha

    • Hormone: IL-8

    • Hormone: IL-12A

      • The correlation between p35 mRNA expression and p70 production accompanied by an overproduction of p40 in LPS-stimulated monocytes implies that the expression of the p35 mRNA is the limiting step in the regulation of IL- 12 production. [5]

      Influenced by:

      • IL-10R-alpha
        in monocyte
        • IL-10 inhibited both IL-12A(p35) and IL-12B(p40) mRNA expression. [5]
        • IL-10 inhibited p35 stronger than p40. [5]

    • Hormone: IL-12B

      Influenced by:

      • IL-4R type l
        in monocyte
        • IL-4 decreased p40 production 8- to 30-fold. [5]
      • IL-10R-alpha
        in monocyte
        • IL-10 inhibited IL-12(p70) completely, and IL-12B(p40) about 10-fold. [5]

    • Hormone: IL-15

    • Hormone: IL-18

    • Hormone: TNF-alpha

      Influenced by:

      • EP4
        in monocyte
        • EP4 receptors are involved in the regulation of TNF-alpha production in monocytes. [6]
        • PGE1, PGE2 and cicaprost suppressed the elaboration of TNF-alpha in LPS-stimulated cells in a concentration-dependent manner. TNF-alpha generation was inhibited by 85 to 90% at the highest concentration (10 mM) of agonist tested. [7]
      • EP2
        in monocyte
        • PGE1, PGE2 and cicaprost suppressed the elaboration of TNF-alpha in LPS-stimulated cells in a concentration-dependent manner. TNF-alpha generation was inhibited by 85 to 90% at the highest concentration (10 mM) of agonist tested. [7]

    • Hormone: IFN-alpha

    • Hormone: CXCL11

      Influenced by:

      • IFNAR2
        in monocyte
        • Induction of CXCL11 by interferon beta. [8]
      • IFNGR1
        in monocyte
        • Induction of CXCL11 by IFN-gamma is enhanced by TNF-alpha in monocytes. [8]

    • Hormone: eotaxin-2

    • Hormone: adipsin

    • Hormone: APRIL

    • Hormone: BAFF

    • Hormone: PD-L1

    • Hormone: IL-19

      • The transscription of the IL-19 mRNA in the monocytes, can be induced by LPS-treatment [9]

    • Hormone: IP-10

    • Hormone: interleukin 6

      Influenced by:

      • IL-4R type l
        in monocyte
        • IL-4 also inhibited IL-I0 and IL-6 production in all donors. [10]
      • IL-10R-alpha
        in monocyte
        • IL-10 inhibited IL-6 production in LPS-stimulated monocytes. [5]

    • Hormone: IL-10

      Influenced by:

      • IL-4R type l
        in monocyte
        • IL-4 also inhibited IL-10 and IL-6 production in all donors. [5]
      • IFNGR1
        in monocyte
        • Both IFN-gamma and IL-4 inhibited IL-I0 production. [5]

    • Hormone: PAF

      Influenced by:

      • CD14
        in monocyte
        • Bacterial lipopolysaccharides (LPS) directly stimulate the synthesis of PAF by a CD14-LPS binding protein (LBP) pathway in monocytes. [11]
      • IL-1RII
        in monocyte
        • IL-1 induce PAF synthesis by monocyte/macrophages. [11]
      • TNFR1
        in monocyte
        • TNF induce PAF synthesis by monocyte/macrophages. [11]

    • Hormone: PGE2

    • Hormone: IL-12

      • Monocytes, macrophages and dendritic cells produce IL-12 in response to a variety of stimuli, including bacterial products. [6]
      • Monocytes are the main IL-12-producing cells in LPS-stimulated human blood. [5]

      Influenced by:

      • IFNGR1
        in monocyte
        • 1000 U/ml IFN-gamma increased Il-12(p70) production 15-fold. [5]
        • Actinobacillus actinomycetemcomitans-LPS alone did not stimulate IL-12 production, a combination of A. actinomycetemcomitans-LPS and IFN-gamma significantly induced IL-12 production in monocytes. [6]
        • In the absence of LPS, IFN-gamma did not induce p70 or p40 production. [5]
      • EP4
        in monocyte
        • PGE2 inhibits IL-12 production via EP4 receptors by monocytes challenged with A. actinomycetemcomitans-LPS and IFN-gamma. [6]
      • IL-10R-alpha
        in monocyte
        • In LPS-stimulated whole blood and purified monocytes, IL-12(p70) and IL-12B(p40) production are enhanced by IFN-gamma and inhibited by IL-10 and IL-4. [5]
        • IL-10 inhibited p70 completely, and p40 about 10-fold. [5]
      • IL-4R type l
        in monocyte
        • The effect of 300 U/ml IL-4 on p70 production varied between donors, resulting in either no effect or a 2-fold decrease in the p70 production. [5]

    • Hormone: soluble VEGFR-1

    • Hormone: resistin

      • Treatment with two independent PPAR-gamma agonists did not change the resistin mRNA levels. [12]

      Influenced by:

      • PPARgamma1
        in monocyte

    • Hormone: FABP4

      Influenced by:

      • PPARgamma1
        in monocyte
        • FABP4, a known PPAR-gamma target, was strikingly increased by 24 h of treatment with two independent PPAR-gamma agonists. [12]

    • Hormone: proteinase 3

    • Hormone: elastase-2

    • Hormone: PAI-2

    • Hormone: interleukin 6

    • Hormone: IL-8

    • Hormone: IL-10

    • Hormone: elafin

    • Hormone: SEMA4D

    Receptors

    • Receptor: CaSR

      Induced phenotype:

      • cytokine secretion
        • The activation of CaSR increases intracellular calcium levels through Gq-PLC-Triphosphate (IP3) pathways and commits to cytokine secretion. [13]

    • Receptor: H3

    • Receptor: IgE Fc receptor gamma-subunit

    • Receptor: H2

    • Receptor: TLR8

    • Receptor: TLR2

      Induced phenotype:

      • monocyte activation
        • We provide evidence that hBD-3 activates cells in a TLR1- and TLR2-dependent manner. [14]
        • hBD-3 induces activation of monocytes and mDCs, but not pDCs or B cells, is consistent with the expected pattern of TLR2 and TLR1 expression on these cells. [14]

    • Receptor: TLR4

    • Receptor: TLR5

    • Receptor: TLR6

    • Receptor: TLR9

    • Receptor: M-CSF-1-R

    • Receptor: thrombospondin receptor

      Induced phenotype:

      • positive regulation of macrophage derived foam cell
        • CD36 binds LDL that has been exposed to "minimally" oxidizing conditions. [15]
        • CD36 has a critical role in monocyte/macrophage foam cell formation and atherosclerosis. [16]

    • Receptor: macrophage-stimulating protein receptor

    • Receptor: IL-10R-alpha

      Influences:

      • IL-12
        • In LPS-stimulated whole blood and purified monocytes, IL-12(p70) and IL-12B(p40) production are enhanced by IFN-gamma and inhibited by IL-10 and IL-4. [5]
        • IL-10 inhibited p70 completely, and p40 about 10-fold. [5]
      • IL-12B
        • IL-10 inhibited IL-12(p70) completely, and IL-12B(p40) about 10-fold. [5]
      • IL-12A
        • IL-10 inhibited both IL-12A(p35) and IL-12B(p40) mRNA expression. [5]
        • IL-10 inhibited p35 stronger than p40. [5]
      • interleukin 6
        • IL-10 inhibited IL-6 production in LPS-stimulated monocytes. [5]

    • Receptor: CD14

      Influences:

      • PAF
        • Bacterial lipopolysaccharides (LPS) directly stimulate the synthesis of PAF by a CD14-LPS binding protein (LBP) pathway in monocytes. [11]

    • Receptor: CCR1

    • Receptor: CCR-2

    • Receptor: CCR5

    • Receptor: CXCR1

    • Receptor: IL-8R B

    • Receptor: CXCR4

    • Receptor: IL-6R

    • Receptor: TNFR1

      Influences:

      • PAF
        • TNF induce PAF synthesis by monocyte/macrophages. [11]

    • Receptor: TLR1

      Induced phenotype:

      • monocyte activation
        • We provide evidence that hBD-3 activates cells in a TLR1- and TLR2-dependent manner. [14]
        • hBD-3 induces activation of monocytes and mDCs, but not pDCs or B cells, is consistent with the expected pattern of TLR2 and TLR1 expression on these cells. [14]

    • Receptor: IFNAR2

      Influences:

      • CXCL11
        • Induction of CXCL11 by interferon beta. [8]

    • Receptor: IFNAR1

    • Receptor: CXCR3

    • Receptor: IFNGR1

      Influences:

      • CXCL11
        • Induction of CXCL11 by IFN-gamma is enhanced by TNF-alpha in monocytes. [8]
      • IL-12
        • 1000 U/ml IFN-gamma increased Il-12(p70) production 15-fold. [5]
        • Actinobacillus actinomycetemcomitans-LPS alone did not stimulate IL-12 production, a combination of A. actinomycetemcomitans-LPS and IFN-gamma significantly induced IL-12 production in monocytes. [6]
        • In the absence of LPS, IFN-gamma did not induce p70 or p40 production. [5]
      • IL-10
        • Both IFN-gamma and IL-4 inhibited IL-I0 production. [5]

    • Receptor: PAF-R

    • Receptor: IL-1RII

      Influences:

      • PAF
        • IL-1 induce PAF synthesis by monocyte/macrophages. [11]

    • Receptor: TLR7

    • Receptor: TLR10

    • Receptor: EP2

      Influences:

      • TNF-alpha
        • PGE1, PGE2 and cicaprost suppressed the elaboration of TNF-alpha in LPS-stimulated cells in a concentration-dependent manner. TNF-alpha generation was inhibited by 85 to 90% at the highest concentration (10 mM) of agonist tested. [7]

    • Receptor: EP4

      Influences:

      • IL-12
        • PGE2 inhibits IL-12 production via EP4 receptors by monocytes challenged with A. actinomycetemcomitans-LPS and IFN-gamma. [6]
      • TNF-alpha
        • EP4 receptors are involved in the regulation of TNF-alpha production in monocytes. [6]
        • PGE1, PGE2 and cicaprost suppressed the elaboration of TNF-alpha in LPS-stimulated cells in a concentration-dependent manner. TNF-alpha generation was inhibited by 85 to 90% at the highest concentration (10 mM) of agonist tested. [7]

    • Receptor: PGI receptor

    • Receptor: EP3

    • Receptor: IL-4R type l

      Influences:

      • IL-12B
        • IL-4 decreased p40 production 8- to 30-fold. [5]
      • IL-12
        • The effect of 300 U/ml IL-4 on p70 production varied between donors, resulting in either no effect or a 2-fold decrease in the p70 production. [5]
      • IL-10
        • IL-4 also inhibited IL-10 and IL-6 production in all donors. [5]
      • interleukin 6
        • IL-4 also inhibited IL-I0 and IL-6 production in all donors. [10]

    • Receptor: CCR3

    • Receptor: IgG Fc receptor I

    • Receptor: interleukin 31 receptor A

    • Receptor: LIR-1

    • Receptor: PSGL-1

    • Receptor: terd

    • Receptor: PPARgamma1

      Influences:

      • FABP4
        • FABP4, a known PPAR-gamma target, was strikingly increased by 24 h of treatment with two independent PPAR-gamma agonists. [12]
      • resistin

    • Receptor: IL-15R alpha

    • Receptor: ADAM17

      Induced phenotype:

      • ectodomain shedding
        • ADAM17 deficient monocytes failed to shed L-selectin in response to PMA. [17]

    • Receptor: ALCAM

    • Receptor: complement C3d receptor

    • Receptor: TCCR

    • Receptor: SIGLEC-7

    • Receptor: FPRL2

    • Receptor: FPRL1

      • FPRL1 is expressed in a great variety of cells including monocytes. [18]

      Induced phenotype:

      • monocyte activation
        • Recently, we found that a G-protein-coupled, seven-transmembrane receptor, FPRL1, mediates the migration and activation of monocytes and microglia induced by Aβ42. [19]

    • Receptor: parathyroid hormone 2 receptor

      • PTH2 receptor is expressed on human granulocytes and--to a lesser degree--on monocytes and lymphocytes [20]
    Reference