Please wait ...

Details for anatomical structure: B-lymphocyte

EndoNet ID: ENC00233

To link to the content of EndoNet use the EndoNet ID that is given on the detail pages in the format ENX0000, where X is a place holder for the type of the component (e. g. R for receptor or C for anatomical structure).
As URL for the linking append this ID to the detail page for this type of component.
For an hormone that would be:

It is also possible to use the search of EndoNet to link to the right detail page. The URL should look like
If the search pattern is unambigious the user is directed to the corresponding detail page.


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


      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]


      • 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


        • 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]