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Details for anatomical structure: B-lymphocyte

EndoNet ID: ENC00233

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Synonyms

B-lymphocyte, bone-marrow-derived lymphocyte, Lymphocytus

General information

lymphocyte; expresses immunoglobulines on its surface; if they get in contact with an antigen, the B-cell differentiates either to a plasma cell, producing antibodies, or to a long-lived memory cell

Links to other resources

Cytomer cy0011317

Larger structures

    Substructures

      Secreted hormones

      • Hormone: IL-12A

      • Hormone: interleukin 6

      • Hormone: MIP-1 beta

      • Hormone: thymosin beta-4

      • Hormone: PD-L1

      • Hormone: IL-12B

      • Hormone: NPY

      • Hormone: stem cell growth factor

      • Hormone: IgE

        Influenced by:

        • IL-4R type l
          in B-lymphocyte
      • Hormone: CD5L

      • Hormone: soluble P-selectin

      • Hormone: TNF-beta

      • Hormone: TNF-C

      • Hormone: IL-1 alpha

      • Hormone: interleukin 6

      • Hormone: IL-10

      • Hormone: TNF-alpha

      • Hormone: SEMA4D

        • The generation of soluble CD100/Sema4D appears to be well regulated; its release from primary B cells is strictly dependent on a proteolytic cascade that follows cellular activation [1]

      Receptors

      • Receptor: PPARgamma1

        • The peroxisome proliferation-activated receptor gamma (PPAR╬│)1 is a member of the nuclear receptor superfamily. It is expressed in many cell types, including adipocytes, epithelial cells, B- and T-cells, macrophages, endothelial cells, neutrophils, and smooth muscle cells [2]
      • Receptor: H1

      • Receptor: H2

      • Receptor: TNFRSF17

        • TNFRSF17 is a nonglycosylated integral membrane type I protein that is preferentially expressed in mature B lymphocytes. [3]

        Induced phenotype:

        • negative regulation of lymphocyte apoptosis
          • TNFRSF17 is a functional member of the TNFR superfamily. It is lacking a "death domain" and its overexpression activates NF-{kappa}B, p38, and JNK. Therefore, upon binding of its corresponding ligand, TNFRSF17 transduces signals for cell survival and proliferation. [4]
      • Receptor: TNFRSF13C

        • TNFRSF13C is a marker of both normal and neoplastic B cells. [5]

        Induced phenotype:

        • negative regulation of B cell apoptosis
          • TNFRSF13C appears to be the principal receptor reqired for BAFF-mediated mature B cell survival and for generating an effective T cell-dependent immune response. [6]
      • Receptor: CD72

        Induced phenotype:

        • B cell response/activation
          • CD100/Sema4D enhances B cell responses by shutting off CD72-mediated negative signalling. [7]
          • CD100/Sema4D-CD72 interaction is a unique example of ligand binding to a negative regulator yielding a positive output. [8]
        • monocyte activation
          • CD100/Sema4D induces immune response through CD72, it appears to play a role in monocyte activation. [9]
          • The negative regulator CD100/Sema4D regulates B cell response through shutting off CD72-mediated negative signaling. [7]
      • Receptor: CCR7

      • Receptor: CD23

      • Receptor: TLR1

      • Receptor: frizzled 3

      • Receptor: IL-10R-alpha

      • Receptor: CCR6

        Induced phenotype:

        • chemotaxis of lymphocytes
          • 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. [10]
      • Receptor: IL-4Ralpha

      • Receptor: IL-2R gamma chain

      • Receptor: IL-4R type l

        Influences:

        • IgE
      • Receptor: TLR4

      • Receptor: B-cell receptor CD22

      • Receptor: LIR-1

      • Receptor: CD7

      • Receptor: IL-18R1

      • Receptor: CD6

      • Receptor: CD5

      • Receptor: RP105

        • cloning of RP105, a novel murine surface molecule that is found exclusively on mature murine B lymphocytes [11]
        • Consistent with the murine RP105, these laboratories describe the presence of transcript in several B cell lines and in B lymphocytes isolated from human tonsil, indicating that the human gene may also be expressed predominantly by B lymphocytes [11]

        Induced phenotype:

        • B-cell activation
          • RP105 may regulate B-cell activation, and RP105-negative B cells produce autoantibodies and take part in pathophysiology of SLE [12]
      • Receptor: complement C3d receptor

      • Receptor: SLAMF1 long form

      • Receptor: TCCR

      • Receptor: ALCAM

      • Receptor: PRLR

      • Receptor: Sphingosine 1-phosphate receptor 1

        Induced phenotype:

        • regulation of leukocyte migration
          • During an antibody response, S1PR1 on IgG-secreting plasma cells is required for the cells to move from the spleen into the blood and, ultimately, to the bone marrow. [13]
          • A similar scenario seems to exist for IgA-producing B cells, which require S1P signalling to migrate out of Peyers patches. [14]
          • In addition to homing to and egress from lymphoid tissues, S1P signalling functions to properly compartmentalize immune cells in lymphoid tissues. An example is the localization and movement of marginal-zone B cells in the spleen, which depend on their expression of S1PR1. [15]
          • S1P signalling has a role in both the homing of immune cells to lymphoid organs, and in controlling their egress into blood and lymph. [16]
          • S1PR1 is decisive for B- cell egress from lymph nodes. [17]
      • Receptor: Sphingosine 1-phosphate receptor 3

      • Receptor: IL-2R

      • Receptor: Programmed cell death protein 1

        • PD-1 is a 55kDa type I transmembrane protein that is upregulated on B cells. [18]

        Induced phenotype:

        • Supression of autoreactive B-lymphocytes
          • PD-1 was identified as the main suppressor of auto-Ab formation (by autoreactive B-cells). [19]
          • We found that B-cells needed to express PD-1 and that T(regulatory)-cells needed to express PD-1 ligands, implying direct communication between T(regs) and B-cells. [19]
      Reference