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Details for anatomical structure: dendritic cell in lymphoid tissues

EndoNet ID: ENC00228

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Synonyms

dendritic cell in lymphoid tissues, , Macrophagocytus stabilis

Links to other resources

Cytomer cy0011307

Larger structures

    Substructures

      Secreted hormones

      • Hormone: pentraxin 3

        • Production of the soluble pattern recognition receptor PTX3 by myeloid, but not plasmacytoid, dendritic cells. [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]
        • 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)). [3]
      • Hormone: IL-18

      • Hormone: MDC

      • Hormone: MIP-3 beta

      • Hormone: PARC

      • Hormone: BAFF

      • Hormone: IL-12

        • DC produce high levels of IL-12, the major cytokine responsible for the generation of inflammatory Th1 cells. [4]

        Influenced by:

        • biliary glycoprotein 1
          in neutrophil_granulocyte
          • 451 Evidence in mice suggests that biliary glycoprotein activation on murine dendritic cells causes IL-6 and IL-12 release. 1410 [5]
      • Hormone: PD-L1

      • Hormone: TNF-alpha

      • Hormone: IL-1 beta

      • Hormone: interleukin 6

      • Hormone: IFN-alpha

        • DCs 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. [6]

        Influenced by:

        • TLR3
          in dendritic_cell_in_lymphoid_tissues
          • TLR3, TLR7, and TLR9 can induce both IFN-alpha and IFN-beta. [7]
        • TLR7
          in dendritic_cell_in_lymphoid_tissues
        • TLR9
          in dendritic_cell_in_lymphoid_tissues
      • Hormone: IFN-beta

        Influenced by:

        • TLR3
          in dendritic_cell_in_lymphoid_tissues
          • TLR3, TLR7, and TLR9 can induce both IFN-alpha and IFN-beta. [7]
        • TLR7
          in dendritic_cell_in_lymphoid_tissues
        • TLR9
          in dendritic_cell_in_lymphoid_tissues
        • TLR4
          in dendritic_cell_in_lymphoid_tissues
          • TLR4 can lead to IFN-beta production. [7]
      • Hormone: IL-29

      • Hormone: RANTES

      • Hormone: IP-10

      • Hormone: IL-10

      • Hormone: IL-1 alpha

      • Hormone: IL-23

      • Hormone: SLAMF1 isoform 3

      • Hormone: IL-8

        Influenced by:

        • TLR3
          in dendritic_cell_in_lymphoid_tissues
          • RNA, likely through secondary structure, is a potent host-derived activator of TLR3. Exposing cells human embryonic kidney 293 cells stably expressing TLR3 and containing a nuclear factor-kB-dependent luciferase reporter) to in vitro transcribed RNA resulted in a TLR3-dependent induction of luciferase activity and interleukin-8 secretion. [8]
      • Hormone: ICAM-1

        • hey showed by flow cytometry and immunohistochemistry that ICAM-1 was widely expressed on different cell types, including tissue macrophages and dendritic cells. It was also expressed on nonhematopoietic cells, such as vascular endothelial cells, thymic and mucosal epithelial cells, and dermal fibroblasts. [9]
      • Hormone: LFA-3

        • The presence of LFA-3 on dendritic cells is consistent with the specialised function of these cells in presenting antigen to effector T-cells. [10]

      Receptors

      • Receptor: H3

      • Receptor: H1

      • Receptor: H2

      • Receptor: histamine H4 receptor

      • Receptor: TLR8

      • Receptor: TLR3

        Influences:

        • IFN-alpha
          • TLR3, TLR7, and TLR9 can induce both IFN-alpha and IFN-beta. [7]
        • IFN-beta
          • TLR3, TLR7, and TLR9 can induce both IFN-alpha and IFN-beta. [7]
        • IL-8
          • RNA, likely through secondary structure, is a potent host-derived activator of TLR3. Exposing cells human embryonic kidney 293 cells stably expressing TLR3 and containing a nuclear factor-kB-dependent luciferase reporter) to in vitro transcribed RNA resulted in a TLR3-dependent induction of luciferase activity and interleukin-8 secretion. [8]
      • Receptor: TLR4

        Influences:

        • IFN-beta
          • TLR4 can lead to IFN-beta production. [7]
      • Receptor: TLR6

      • Receptor: TLR9

        Influences:

        • IFN-alpha
        • IFN-beta
      • Receptor: SIGLEC-7

      • Receptor: PAF-R

      • Receptor: TLR7

        Influences:

        • IFN-alpha
        • IFN-beta
      • Receptor: LIR-1

      • Receptor: CD5

      • Receptor: CD72

        Influences:

        • IFN-gamma
          • Activated NK cells express CD100 and produce soluble CD100. They interact with dendritic cells 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. [11]
        • SEMA4D
          • Activated NK cells express CD100 and produce soluble CD100. They interact with dentritic cells 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. [11]
      • Receptor: Sphingosine 1-phosphate receptor 1

        Induced phenotype:

        • dendritic cell chemotaxis
          • FTY720, a S1P receptor agonist, can severly hamper migration of dendritic cells to the lymph nodes suggesting additional mechanisms underlying the immunosuppressive effects of this spingosine analog. [12]
      • Receptor: Sphingosine 1-phosphate receptor 2

      • Receptor: Sphingosine 1-phosphate receptor 3

        Induced phenotype:

        • dendritic cell chemotaxis
          • DCs mainly express S1PR1 when immature but on maturation upregulate S1PR3, which then seems to mediate a chemotatic response to S1P. [13]
        • positive regulation of endocytosis
          • S1P has been shown to increase endocytosis by mature DCs through S1PR3 engagement. [14]
          • This S1P-mediated enhancement of endocytosis in mature DCs could be involved in the removal of bacteria during infection. [14]
        • positive regulation of interleukin-1 beta production
          • S1PR3 is essential for inducing the production of IL-1beta and tissue factor and for their dissemination into the lung circulation, thereby amplifying inflammation and coagulation. [15]
      • Receptor: Sphingosine 1-phosphate receptor 4

        Induced phenotype:

        • regulation of T cell differentiation
          • S1P has been shown to modulate the polarizing functions of DCs on T cells when exposed to bacterial products. [16]
        • regulation of leukocyte migration
          • S1PR4 is dominantly expressed on mouse dendritic cells and has an important role in DC trafficking. [17]
        • dendritic cell chemotaxis
          • FTY720, a S1P receptor agonist, can severly hamper migration of dendritic cells to the lymph nodes suggesting additional mechanisms underlying the immunosuppressive effects of this spingosine analog. [12]
      • Receptor: Sphingosine 1-phosphate receptor 5

        Induced phenotype:

        • dendritic cell chemotaxis
          • FTY720, a S1P receptor agonist, can severly hamper migration of dendritic cells to the lymph nodes suggesting additional mechanisms underlying the immunosuppressive effects of this spingosine analog. [12]
      • Receptor: Lysophosphatidic acid receptor 3

        Induced phenotype:

        • dendritic cell chemotaxis
          • LPA3 activation induced chemotaxis of immature, but not mature, DCs. [18]
      • Receptor: Probable G-protein coupled receptor 132

        Induced phenotype:

        • regulation of innate immune response
          • 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. [19]
      • Receptor: CMKLR1

        • We have previously described ChemR23 as a human orphan G protein–coupled receptor expressed in macrophages and immature DCs [20]

        Induced phenotype:

        • dendritic cell chemotaxis
          • Human recombinant chemerin promoted in vitro migration of immature DCs whereas no chemotaxis of mature DCs was observed [20]
      • Receptor: CCR6

        • human CCR6, a chemokine receptor preferentially expressed by immature dendritic cells and memory T cells. [21]

        Induced phenotype:

        • dendritic cell chemotaxis
          • β-defensins may promote adaptive immune responses by recruiting dendritic and T cells to the site of microbial invasion through interaction with CCR6. [21]
          • CC-chemokine receptor (CCR) 6 is the only known receptor for macrophage inflammatory protein (MIP)-3alpha, a CC chemokine chemotactic for lymphocytes and dendritic cells. [22]
      • Receptor: CCR7

        • Chemokine receptor CCR7 is expressed on mature DC. [23]

        Induced phenotype:

        • dendritic cell chemotaxis
          • Migration of DC to lymph nodes is regulated by chemokine receptor CCR7, expressed on mature DC, and the CCR7 ligands CCL19 and CCL21. [23]
      Reference