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Details for anatomical structure: macrophage

EndoNet ID: ENC00216

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Synonyms

macrophage, , Macrophagocytus

General information

cellular phagocytosis immune reaction

Links to other resources

Cytomer cy0011303

Larger structures

    Substructures

      Secreted hormones

      • Hormone: ADM

      • Hormone: pentraxin 3

        • PTX3 is made by diverse cell types, most prominently endothelial cells, macrophages and dendritic cells, in response to primary inflammatory signals (e.g. interleukin-1 (IL-1), tumour necrosis factor (TNF), lipopolysaccharide (LPS)). [1]
        • PTX3 is produced by a variety of cells and tissues, most notably dendritic cells and macrophages, in response to Toll-like receptor (TLR) engagement and inflammatory cytokines. [2]
      • Hormone: TNF-alpha

        • In man, the secretion of TNFalpha is reported to be mainly due to the cells of the stromal vascular and matrix fractions, including the macrophages. [3]

        Influenced by:

        • TLR2
          in alveolar_macrophage
          • SP-A significantly reduced PGN-elicited tumor necrosis factor alpha (TNF-alpha) secretion by rat alveolar macrophages. The inhibitory effect on TNF-alpha secretion was dependent upon SP-A concentrations in physiological range. [4]
          • Direct interaction of SP-A with TLR2 alters PGN-induced cell signaling. [4]
      • Hormone: MIG

      • Hormone: IL-18

      • Hormone: IL-12A

      • Hormone: C-C motif chemokine 2

      • Hormone: GRObeta

      • Hormone: MDC

      • Hormone: IL-1F5

      • Hormone: PARC

        • Specifically induced in macrophages by IL-4, IL-13, and IL-10. Expression is inhibited by IFN-gamma while glucocorticoids exert a slightly positive synergistic effect in combination with IL-4. [6]
      • Hormone: resistin

        • Human resistin mRNA and protein were found to be expressed in human primary monocyte-derived macrophages, and levels were downregulated after 96-h treatment with rosiglitazone. [7]
      • Hormone: adipsin

      • Hormone: eotaxin

        • Human eotaxin is an 8,3-kDa, 74-amino-acid residue, nonglycosylated polypeptide secreted by endothelial cells, fibroblasts, macrophages, ciliated and nonciliated bronchial epithelial cells, smooth muscle cells, chondrocytes, and eosinophils. [8]
      • Hormone: CD40-L

      • Hormone: tenascin-C

      • Hormone: APRIL

      • Hormone: BAFF

      • Hormone: thymosin beta-4

      • Hormone: TIMP-1

      • Hormone: osteopontin

        • Osteopontin is exceptionally highly expressed in adipose tissue macrophages in humans and mice. [9]
      • Hormone: IFN-beta

        • Human monocyte-derived macrophages express IFN-alpha, IFN-beta, IL-28, IL-29, TNF-alpha and the chemokines CCL5 and CXCL10 after herpes simplex virus 1 (HSV-1) infection. [10]

        Influenced by:

        • TLR4
          in macrophage
          • With LPS in the presence of LPS-binding protein TLR4 activates the common MyD88-dependent signaling pathway as well as a MyD88-independent pathway leading to interferon-beta production. [11]
      • Hormone: interleukin 6

      • Hormone: IFN-alpha

        Influenced by:

        • TLR4
          in macrophage
      • Hormone: IP-10

      • Hormone: IL-29

      • Hormone: RANTES

      • Hormone: IL-10

      • Hormone: IL-1 alpha

      • Hormone: PAF

        Influenced by:

        • TNFR1
          in macrophage
          • TNF induce PAF synthesis by monocyte/macrophages. [12]
        • IL-1RII
          in macrophage
          • IL-1 induce PAF synthesis by monocyte/macrophages. [12]
      • Hormone: IL-12

      • Hormone: FGF-2

      • Hormone: CD5L

      • Hormone: elastase-2

      • Hormone: elafin

      • Hormone: TXA2

      • Hormone: ATP-binding cassette sub-family A member 1

      • Hormone: APOE

        Influenced by:

        • ApoA-I receptor
          in macrophage
          • ApoA-I stimulates secretion of apoE from macrophage foam cells, although the mechanism of this process is not understood. [13]
          • ApoA-I stimulates secretion of apoE independently of both ABCA1-mediated cholesterol efflux and of lipid binding by its terminus. [13]
      • Hormone: cholesterol

        Influenced by:

        • ATP-binding cassette sub-family A member 1
          in macrophage
          • It is likely that ABCA1 is the cAMP-inducible apolipoprotein receptor that promotes secretion of lipids from macrophages. [14]
          • There was an investigation whether ABCA1 expression is also responsible for the apoA-I-mediated cholesterol efflux induced by cAMP in macrophages and whether this involves direct binding of apoA-I to plasma membrane ABCA1. [14]
      • Hormone: TGF-beta 1

        • Subtype THP-1 cells secrete TGF-beta1 into the medium by forming a functional complex with the latent TGF-beta1-binding protein. We conclude that subtype THP-1 cells could not take up Ac-LDL because ScR was inhibited (leading to a loss of function) caused by the secreted TGF-beta1. [15]
      • Hormone: CCL1

        Influenced by:

        • AhR
          in macrophage
          • Polycyclic aromatic hydrocarbons (PAHs) induce expression of the chemokine CCL1 in an AhR- and calcium-dependent manner. [16]
      • Hormone: IL-1 beta

        • IL-1β is abundantly secreted by activated macrophages and blood monocytes. [17]
        • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
        • Pro-IL-1β is then cleaved by caspase- to biologically-active mature IL-1β. [18]

        Influenced by:

        • TLR4
          in macrophage
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
        • TLR8
          in macrophage
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
        • TLR9
          in macrophage
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
        • TLR7
          in macrophage
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
        • TLR10
          in macrophage
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
        • TLR6
          in macrophage
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
        • TLR2
          in macrophage
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
        • TLR3
          in macrophage
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
        • TLR5
          in macrophage
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
        • TLR1
          in macrophage
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
      • Hormone: MMP-3

        Influenced by:

        • basigin
          in brain
          • CD147/Basigin induces matrix metalloproteinase expression in neighbouring fibroblasts, leading to tumor cell invasion [19]
      • Hormone: MMP-7

      • Hormone: ICAM-1

      Receptors

      • Receptor: glucocorticoid receptor

        Induced phenotype:

        • hypertension
          • Oxidative stress and nitric oxide deficiency are emerging as key components in the pathogenesis of glucocorticoid-induced hypertension. [20]
          • This highlights the role of inflammation and oxidative stress in the pathogenesis of glucocorticoid-induced hypertension and this is consistent with a role for macrophages in this pathology. [21]
        • abdominal obesity-metabolic syndrome
          • Glucocorticoids play a role in adipocyte maturation, function and distribution. Differentiating adipocytes produce increasing levels of the enzyme 11-beta-hydroxysteroid dehydrogenase 1 to convert inactive cortisone into cortisol, in turn amplifying local glucocorticoid levels. [22]
          • Many findings implicate macrophages, GR and 11βHSD1 in the pro-inflammatory phenotype of metabolic dysfunction. [21]
        • negative regulation of immune response
          • A recent study exploring the effect of corticosterone on isolated peritoneal macrophages has demonstrated that high corticosterone concentrations suppress macrophage immune functions. [23]
          • Responses to high corticosteroid levels are a consequence of GR activation. [23]
        • osteoporosis
          • Glucocorticoids suppress osteoblast activity in vivo. [24]
          • Glucocorticoid signalling via GR inhibits proliferation of osteoclastogenic cells, apoptosis of mature osteoclasts and osteoclast function in vitro and in vivo, by altering the activity rather than the number of osteoclasts. Glucocorticoid-induced bone mass reduction is not only mediated by directly inhibiting osteoblasts, but also by inhibiting osteoclast activity, which in turn disrupts the remodelling cycle and suppresses osteoblast activity . [25]
        • atherosclerosis
          • Atherosclerosis is a progressive disease characterised by an inflammatory event in which monocyte-derived macrophages play a central role. [26]
          • Glucocorticoid treatment has been shown to reduce macrophage accumulation in a model of cholesterol-induced atherosclerosis. [27]
          • Glucocorticoid treatment has been shown to decrease neointimal proliferation following balloon angioplasty. [28]
          • Effects of glucocorticoids on etiology and progression of atherosclerosis are only partially mediated through GR. [21]
      • Receptor: GR-beta

      • Receptor: PPARgamma1

        • The peroxisome proliferation-activated receptor gamma (PPARγ) is expressed in many cell types including mammary epithelium, ovary, macrophages, and B- and T-cells [29]
      • Receptor: TLR4

        Influences:

        • IFN-beta
          • With LPS in the presence of LPS-binding protein TLR4 activates the common MyD88-dependent signaling pathway as well as a MyD88-independent pathway leading to interferon-beta production. [11]
        • IFN-alpha
        • IL-1 beta
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
      • Receptor: ferroportin-1

      • Receptor: PPAR-gamma1

      • Receptor: vitronectin receptor

        Induced phenotype:

        • positive regulation of macrophage derived foam cell
          • AlphaVbeta3 integrin regulates macrophage functional maturation into foam cells in a persistent manner [30]
      • Receptor: LXR-alpha

      • Receptor: basigin

      • Receptor: LRP5

      • Receptor: TNFR1

        Influences:

        • PAF
          • TNF induce PAF synthesis by monocyte/macrophages. [12]
      • Receptor: PAF-R

      • Receptor: IL-1RII

        Influences:

        • PAF
          • IL-1 induce PAF synthesis by monocyte/macrophages. [12]
      • Receptor: IgE Fc receptor, alpha-subunit

      • Receptor: IL-15R alpha

      • Receptor: ADAM17

      • Receptor: sialoadhesin

        Induced phenotype:

        • cell-cell interactions of macrophages during inflammatory reactions
          • aken together, these observations indicate that Sn has evolved primarily to mediate extracellular functions, namely cell-cell or cell-matrix interactions. [31]
      • Receptor: MRC2

      • Receptor: ApoA-I receptor

        Influences:

        • APOE
          • ApoA-I stimulates secretion of apoE from macrophage foam cells, although the mechanism of this process is not understood. [13]
          • ApoA-I stimulates secretion of apoE independently of both ABCA1-mediated cholesterol efflux and of lipid binding by its terminus. [13]
      • Receptor: ATP-binding cassette sub-family A member 1

        Influences:

        • cholesterol
          • It is likely that ABCA1 is the cAMP-inducible apolipoprotein receptor that promotes secretion of lipids from macrophages. [14]
          • There was an investigation whether ABCA1 expression is also responsible for the apoA-I-mediated cholesterol efflux induced by cAMP in macrophages and whether this involves direct binding of apoA-I to plasma membrane ABCA1. [14]
      • Receptor: AhR

        Influences:

        • CCL1
          • Polycyclic aromatic hydrocarbons (PAHs) induce expression of the chemokine CCL1 in an AhR- and calcium-dependent manner. [16]
      • Receptor: TLR8

        Influences:

        • IL-1 beta
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
      • Receptor: TLR9

        Influences:

        • IL-1 beta
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
      • Receptor: TLR7

        Influences:

        • IL-1 beta
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
      • Receptor: TLR10

        Influences:

        • IL-1 beta
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
      • Receptor: TLR6

        Influences:

        • IL-1 beta
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
      • Receptor: TLR2

        Influences:

        • IL-1 beta
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
      • Receptor: TLR3

        Influences:

        • IL-1 beta
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
      • Receptor: TLR5

        Influences:

        • IL-1 beta
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
      • Receptor: TLR1

        Influences:

        • IL-1 beta
          • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [18]
      • Receptor: CD72

        Induced phenotype:

        • macrophage activation during immune response
          • CD100/Sema4D induces immune response through CD72, it appears to play a role in monocyte activation. [32]
          • The negative regulator CD100/Sema4D regulates B cell response through shutting off CD72-mediated negative signaling. [33]

        Influences:

        • IFN-gamma
          • Activated NK cells express CD100 and produce soluble CD100. They interact with macrophages by several routs among which is the CD100-CD72 interaction. Such interaction lead to IFNgamma secretion which in turn activates other cells of the immune system. [34]
        • SEMA4D
          • Activated NK cells express CD100 and produce soluble CD100. They interact with macrophages by several routs among which is the CD100-CD72 interaction. Such interaction lead to soluble CD100 secretion which in turn activates other cells of the immune system. [34]
      • Receptor: PRLR

        Induced phenotype:

        • macrophage activation during immune response
          • It has been shown that macrophage activation and superoxide anion production responsible for killing pathogenic organisms are effects mediated by the PRLR. [35]
          • Activation of macrophages was originally thought to be an action of GH. However, it has been shown that macrophage activation is an effect mediated by the prolactin receptor. [36]
      • Receptor: Sphingosine 1-phosphate receptor 1

        Induced phenotype:

        • negative regulation of cytokine production
          • Peritoneal macrophages from low-density lipoprotein-receptor-deficient mice, which are a model for atherosclerosis, that had been treated with FTY720 (FTY720 is a sphingosine analogue that could be phosphorylated by SPHKs to produce a S1PR ligand with potent effects, including S1PR agonism and the downregulation of S1PR expression) had a markedly decreased production of inflammatory tumour-necrosis factor (TNF), TNF receptor (TNFR) and IL-6 in response to LPS. [37]
      • Receptor: Sphingosine 1-phosphate receptor 2

        Induced phenotype:

        • negative regulation of cytokine production
          • Peritoneal macrophages from low-density lipoprotein-receptor-deficient mice, which are a model for atherosclerosis, that had been treated with FTY720 (FTY720 is a sphingosine analogue that could be phosphorylated by SPHKs to produce a S1PR ligand with potent effects, including S1PR agonism and the downregulation of S1PR expression) had a markedly decreased production of inflammatory tumour-necrosis factor (TNF), TNF receptor (TNFR) and IL-6 in response to LPS. [37]
      • Receptor: Probable G-protein coupled receptor 132

        Induced phenotype:

        • regulation of innate immune response
          • 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. [38]
        • atherosclerosis
          • The key role of LPC as a major antigenic component of oxLDL has implicated this bioactive lipid in atherosclerosis, the primary cause of heart disease and stroke. [38]
          • Aspects of immune function as potential targets of LPC action play some role in atherogenesis. Macrophage responses to oxLDL such as migration and activation are likely determined to a significant extent by its LPC content, and may therefore be mediated to some degree via G2A and/or GPR4. [38]
      • Receptor: G-protein coupled receptor 4

        Induced phenotype:

        • atherosclerosis
          • The key role of LPC as a major antigenic component of oxLDL has implicated this bioactive lipid in atherosclerosis, the primary cause of heart disease and stroke. [38]
          • Aspects of immune function as potential targets of LPC action play some role in atherogenesis. Macrophage responses to oxLDL such as migration and activation are likely determined to a significant extent by its LPC content, and may therefore be mediated to some degree via G2A and/or GPR4. [38]
      • Receptor: Psychosine receptor

        Induced phenotype:

        • Krabbe disease
          • The secondary accumulation of Psy in macrophages probably induces the formation of globoid cells. [39]
      • Receptor: mineralcorticoid receptor

        Induced phenotype:

        • positive regulation of immune response
          • A recent study exploring the effect of corticosterone on isolated peritoneal macrophages has demonstrated that low corticosterone concentrations enhance macrophage immune functions. [23]
          • The effects of low corticosterone concentrations are mediated via MR. [23]
        • fibrosis
          • In renal disease models, reduced monocyte/macrophage infiltration is accompanied by a substantial reduction in fibrosis. MR signalling and macrophages appear to be important in inflammatory conditions in the kidney. [21]
          • Activation of an MR, in the context of inappropriate sodium status, has major cardiovascular pathophysiological consequences including cardiac fibrosis. [21]
          • In cardiac disease models, reduced monocyte/macrophage infiltration is accompanied by a substantial reduction in fibrosis. MR signalling and macrophages appear to be important in inflammatory conditions in the heart. [21]
          • Selective deletion of MR from macrophages protected against mineralocorticoid-mediated cardiac fibrosis, despite normal macrophage recruitment. [21]
        • production of molecular mediator involved in inflammatory
          • Inflammation may be a key mechanism translating MR signalling into cardiac and vascular remodelling. [21]
          • Mineralocorticoid/salt-induced pathology is characterised by an early vascular inflammatory response with elevated cardiac expression of inflammatory mediators such as monocytes/macrophages, MCP-1 and adhesion molecules (ICAM-1 and VCAM-1), prior to the onset of collagen deposition. [40]
          • mineralocorticoid/salt treatment is also associated with increased monocyte/macrophage infiltration and expression of inflammatory markers such as osteopontin, MCP-1, IL-6 and IL-1β in the kidney. [41]
          • MR antagonism prevents inflammation-induced peritoneal fibrosis and reduces macrophage infiltration and expression of MCP-1, TGF-β, PAI-1 and Sgk-1. [42]
        • atherosclerosis
          • Aldosterone treatment increases oxidative stress in macrophages derived from ApoE-deficient mice. [43]
          • Aldosterone activation of MR in endothelial cells specifically modulates ICAM-1 expression and promotes leukocyte adhesion, supporting a role for MR signalling in endothelial cells in the initial stages of atherosclerosis. These findings highlight a key role for both macrophage and endothelial MR signalling in atherosclerosis. [44]
        • hypertension
          • Activation of an MR, in the context of inappropriate sodium status, has major cardiovascular pathophysiological consequences including hypertension. [21]
          • Chronic inappropriate activation of an MR is well recognised to promote hypertension. Excess plasma mineralocorticoids promote sodium and water retention and potassium secretion leading to the maintenance of blood pressure at a higher set point. [45]
          • MR antagonists have been shown to be effective anti-hypertensive agents in essential hypertension, suggesting a role for MR signalling in hypertension. [46]
      • Receptor: ER-alpha

        Induced phenotype:

        • regulation of inflammatory response
          • ER alpha is critical for maintenance of macrophage metabolism and for macrophage IL-4 responsiveness. [47]
          • ER alpha is necessary for the repression of inflammation, maintenance of oxidative metabolsim and full phagocytic activity in isolated macrophages. [47]
      • Receptor: progesterone receptor

      • Receptor: VDR

        Induced phenotype:

        • negative regulation of macrophage derived foam cell differentiation
          • Activation of vitamin D receptor signaling prevents foam cell formation by reducing modified LDL cholesterol uptake in macrophages. [48]
      • Receptor: thyroid hormone receptor beta 2

      • Receptor: THRB1

      • Receptor: THRA1

      • Receptor: thyroid hormone receptor alpha2

      • Receptor: RAR

        Induced phenotype:

        • Positive regulator of inflammatory cytokine production
          • Inflammatory cytokine production is impaired in RAR-deficient macrophages. [49]
      • Receptor: RAR-beta

      • Receptor: RXR-alpha

      • Receptor: CMKLR1

        • We have previously described ChemR23 as a human orphan G protein–coupled receptor expressed in macrophages and immature DCs [50]

        Induced phenotype:

        • chemotaxis of macrophages
          • Human recombinant chemerin promoted in vitro migration of macrophages was observed. [50]
      Reference