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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

    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