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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

  • circulatory_system__hematopoietic_system
  • parts_of_human_body
  • digestive_system
  • lymph_node
  • tonsil
  • immune_system
  • lymphoid_tissue
  • blood
  • spleen
  • liver
  • bone_marrow

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 (PPARγ)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