User:Darganm/sandbox
Introduction
[edit]CD79 (Cluster of Differentiation 79) is a transmembrane protein that forms a complex with the B-cell receptor (BCR) and generates a signal following recognition of antigen by the BCR. CD79 is composed of two distinct chains called CD79A and CD79B (formerly known as Ig-alpha and Ig-beta); these form a heterodimer on the surface of a B cell stabilized by disulfide bonding.[1] CD79a and CD79b are both members of the immunoglobulin superfamily. Human CD79a is encoded by the mb-1 gene that is located on chromosome 19, and CD79b is encoded by the B29 gene that located on chromosome 17.[1][2] Both CD79 chains contain an immunoreceptor tyrosine-based activation motif (ITAM) in their intracellular tails that they use to propagate a signal in a B cell, in a similar manner to CD3-generated signal tranduction observed during T cell receptor activation on T cells.[3]
Function
[edit]CD79 serves to be a pan-B cell marker for the detection of B-cell neoplasms. However, tumor cells in some cases of T-lymphoblastic leukemia/lymphoma and AML has shown to potentially react positively with CD79 monoclonal antibodies. [4] In addition, both CD79 chains contain an immunoreceptor tyrosine-based activation motif (ITAM), which some scientists have found to propagate downstream signaling in B-cells. CD79 has been tested as a B-cell target in MRL/lpr mice, a mouse model for systemic lupus erythematosus (SLE). [5] CD79, expressed by B-cell and plasma cell precursors is a candidate that induces apoptosis as well as inhibition of B-cell receptor (BCR) activation and possibly depletion of ectopic germinal centers (GC). [5] However, research on CD79 still remains very open.
CD79 and BCR Signalling
[edit]Scientists identified mutations in the BCR coreceptor CD79A/B that lead to chronic activation of BCR signaling. Somatic mutations affecting the ITAM signalling modules of CD79B and CD79A were detected frequently in biopsy samples. [6] Moreover, some researchers believe that CD79 may emerge as an alternative target for the treatment of B-cell-dependent autoimmunity.[7] Hardy et al. found that upon an Ag-induced BCR aggregation, CD79 is phosphorylated and initiates a cascade of downstream signaling events. Hardy et al. further characterized an alternate mode of BCR signaling that is induced by chronic AgR stimulation and maintains a state of B cell unresponsiveness termed "anergy".[8] Other studies that focused on the deficiencies observed in neonatal antibody production can be due to various intrinsic features such as B-cell immaturity, poor B-cell repertoire or reduced strength of BCR signaling. Activation of the BCR with T-cell-dependent (TD) or TI antigens induces cross-linking of surface Ig molecules and binding to the transmembrane protein CD79. <---- work on this
https://search.proquest.com/docview/1553746775?accountid=9892&rfr_id=info%3Axri%2Fsid%3Aprimo
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- ^ a b Chu P, Arber D (2001). "CD79: a review". Appl Immunohistochem Mol Morphol. 9 (2): 97–106. doi:10.1097/00022744-200106000-00001. PMID 11396639.
- ^ Van Noesel C, Brouns G, van Schijndel G, Bende R, Mason D, Borst J, van Lier R (1992). "Comparison of human B cell antigen receptor complexes: membrane- expressed forms of immunoglobulin (Ig)M, IgD, and IgG are associated with structurally related heterodimers". J Exp Med. 175 (6): 1511–9. doi:10.1084/jem.175.6.1511. PMC 2119249. PMID 1375264.
- ^ Müller B, Cooper L, Terhorst C (1995). "Interplay between the human TCR/CD3 epsilon and the B-cell antigen receptor associated Ig-beta (B29)". Immunol Lett. 44 (2–3): 97–103. doi:10.1016/0165-2478(94)00199-2. PMID 7541024.
- ^ Naeim, Faramarz; Rao, P. Nagesh; Song, Sophie X.; Grody, Wayne W. Principles of Immunophenotyping. pp. 25–46. doi:10.1016/b978-0-12-385183-3.00002-4.
- ^ a b Nakken, Britt; Munthe, Ludvig A.; Konttinen, Yrjö T.; Sandberg, Anna Klokk; Szekanecz, Zoltan; Alex, Philip; Szodoray, Peter. "B-cells and their targeting in rheumatoid arthritis — Current concepts and future perspectives". Autoimmunity Reviews. 11 (1): 28–34. doi:10.1016/j.autrev.2011.06.010.
- ^ Davis, R. Eric; Ngo, Vu N.; Lenz, Georg; Tolar, Pavel; Young, Ryan M.; Romesser, Paul B.; Kohlhammer, Holger; Lamy, Laurence; Zhao, Hong (2010/01). "Chronic active B-cell-receptor signalling in diffuse large B-cell lymphoma". Nature. 463 (7277): 88–92. doi:10.1038/nature08638. ISSN 1476-4687.
{{cite journal}}: Check date values in:|date=(help) - ^ Li, Yongmei; Chen, Fangqi; Putt, Mary; Koo, Yumee K.; Madaio, Michael; Cambier, John C.; Cohen, Philip L.; Eisenberg, Robert A. (2008-09-01). "B Cell Depletion with Anti-CD79 mAbs Ameliorates Autoimmune Disease in MRL/lpr Mice". Journal of immunology (Baltimore, Md. : 1950). 181 (5): 2961–2972. ISSN 0022-1767. PMC 2865432. PMID 18713966.
{{cite journal}}: CS1 maint: PMC format (link) - ^ Hardy, Ian R.; Anceriz, Nadia; Rousseau, François; Seefeldt, Matt B.; Hatterer, Eric; Irla, Magali; Buatois, Vanessa; Chatel, Laurence E.; Getahun, Andrew (2014-02-15). "Anti-CD79 Antibody Induces B Cell Anergy That Protects against Autoimmunity". The Journal of Immunology. 192 (4): 1641–1650. doi:10.4049/jimmunol.1302672. ISSN 0022-1767. PMID 24442438.