- CD154
CD154, also called CD40 ligand or CD40L, is a protein that is primarily expressed on activated
T cells and is a member of theTNF family of molecules. It binds toCD40 onantigen-presenting cells (APC), which leads to many effects depending on the target cell type. In general, CD40L plays the role of a costimulatory molecule and induces activation in APC in association with T cell receptor stimulation by MHC molecules on the APC. PBB_Summary
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summary_text = The protein encoded by this gene is expressed on the surface of T cells. It regulates B cell function by engaging CD40 on the B cell surface. A defect in this gene results in an inability to undergo immunoglobulin class switch and is associated with hyper-IgM syndrome. [cite web | title = Entrez Gene: CD40LG CD40 ligand (TNF superfamily, member 5, hyper-IgM syndrome)| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=959| accessdate = ]Expression of CD154
CD40 ligand is primarily expressed on activated CD4+ T lymphocytes but is also found in a soluble form. While CD40L was originally described on T lymphocytes, its expression has since been found on a wide variety of cells, including platelets, mast cells, macrophages, basophils, NK cells, B lymphocytes, as well as non-haematopoietic cells (smooth muscle cells, endothelial cells, and epithelial cells) [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=11229815&query_hl=1&itool=pubmed_docsum] .
pecific effects on cells
Macrophages
In the
macrophage , the primary signal for activation is IFN-γ from Th1 typeCD4 T cells. The secondary signal is CD40L on the T cell, which bindsCD40 on themacrophage cell surface. As a result, the macrophage expresses more CD40 andTNF receptors on its surface, which helps increase the level of activation. The activated macrophage can then destroy phagocytosed bacteria and produce more cytokines.B cells
The
B cell can presentantigens to helper T cells. If theT cell recognizes the peptide presented by the B cell, the T cell synthesizes CD40L. The CD40L binds to the B cell's CD40 receptor, causing resting B cell activation. The T cell also producesIL-4 , which directly binds to B cell receptors. As a result of this interaction, the B cell can undergo division,antibody isotype switching , and differentiation to plasma cells. The end-result is a B cell that is able to mass-produce specific antibodies against an antigenic target.References
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Further reading
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citations =
*cite journal | author=Tong AW, Stone MJ |title=CD40 and the effect of anti-CD40-binding on human multiple myeloma clonogenicity. |journal=Leuk. Lymphoma |volume=21 |issue= 1-2 |pages= 1–8 |year= 1997 |pmid= 8907262 |doi=
*cite journal | author=van Kooten C, Banchereau J |title=CD40-CD40 ligand. |journal=J. Leukoc. Biol. |volume=67 |issue= 1 |pages= 2–17 |year= 2000 |pmid= 10647992 |doi=
*cite journal | author=Schattner EJ |title=CD40 ligand in CLL pathogenesis and therapy. |journal=Leuk. Lymphoma |volume=37 |issue= 5-6 |pages= 461–72 |year= 2003 |pmid= 11042507 |doi=
*cite journal | author=Bhushan A, Covey LR |title=CD40:CD40L interactions in X-linked and non-X-linked hyper-IgM syndromes. |journal=Immunol. Res. |volume=24 |issue= 3 |pages= 311–24 |year= 2002 |pmid= 11817328 |doi=
*cite journal | author=Cheng G, Schoenberger SP |title=CD40 signaling and autoimmunity. |journal=Curr. Dir. Autoimmun. |volume=5 |issue= |pages= 51–61 |year= 2002 |pmid= 11826760 |doi=
*cite journal | author=Subauste CS |title=CD154 and type-1 cytokine response: from hyper IgM syndrome to human immunodeficiency virus infection. |journal=J. Infect. Dis. |volume=185 Suppl 1 |issue= |pages= S83–9 |year= 2002 |pmid= 11865444 |doi=
*cite journal | author=Kornbluth RS |title=An expanding role for CD40L and other tumor necrosis factor superfamily ligands in HIV infection. |journal=J. Hematother. Stem Cell Res. |volume=11 |issue= 5 |pages= 787–801 |year= 2003 |pmid= 12427285 |doi= 10.1089/152581602760404595
*cite journal | author=Xu Y, Song G |title=The role of CD40-CD154 interaction in cell immunoregulation. |journal=J. Biomed. Sci. |volume=11 |issue= 4 |pages= 426–38 |year= 2005 |pmid= 15153777 |doi= 10.1159/000077892External links
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