(Redirected from CD79a)
Jump to: navigation, search
CD79a molecule, immunoglobulin-associated alpha
Alt. symbolsIG-alpha
Other data
LocusChr. 19 q13.2


CD79b molecule, immunoglobulin-associated beta
Alt. symbolsIG-beta
Other data
LocusChr. 17 q23

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 transduction observed during T cell receptor activation on T cells.[3]


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 Signaling

Scientists identified mutations in the BCR coreceptor CD79A/B that lead to chronic activation of BCR signaling. Somatic mutations affecting the ITAM signaling 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.


  1. 1.0 1.1 Chu PG, Arber DA (June 2001). "CD79: a review". Applied Immunohistochemistry & Molecular Morphology. 9 (2): 97–106. doi:10.1097/00022744-200106000-00001. PMID 11396639.
  2. Van Noesel CJ, Brouns GS, van Schijndel GM, Bende RJ, Mason DY, Borst J, van Lier RA (June 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". The Journal of Experimental Medicine. 175 (6): 1511–9. doi:10.1084/jem.175.6.1511. PMC 2119249. PMID 1375264.
  3. Müller B, Cooper L, Terhorst C (January 1995). "Interplay between the human TCR/CD3 epsilon and the B-cell antigen receptor associated Ig-beta (B29)". Immunology Letters. 44 (2–3): 97–103. doi:10.1016/0165-2478(94)00199-2. PMID 7541024.
  4. Naeim F, Rao PN, Song SX, Grody WW. Principles of Immunophenotyping. pp. 25–46. doi:10.1016/b978-0-12-385183-3.00002-4.
  5. 5.0 5.1 Nakken B, Munthe LA, Konttinen YT, Sandberg AK, Szekanecz Z, Alex P, Szodoray P (November 2011). "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. PMID 21777703.
  6. Davis RE, Ngo VN, Lenz G, Tolar P, Young RM, Romesser PB, Kohlhammer H, Lamy L, Zhao H, Yang Y, Xu W, Shaffer AL, Wright G, Xiao W, Powell J, Jiang JK, Thomas CJ, Rosenwald A, Ott G, Muller-Hermelink HK, Gascoyne RD, Connors JM, Johnson NA, Rimsza LM, Campo E, Jaffe ES, Wilson WH, Delabie J, Smeland EB, Fisher RI, Braziel RM, Tubbs RR, Cook JR, Weisenburger DD, Chan WC, Pierce SK, Staudt LM (January 2010). "Chronic active B-cell-receptor signalling in diffuse large B-cell lymphoma". Nature. 463 (7277): 88–92. doi:10.1038/nature08638. PMC 2845535. PMID 20054396.
  7. Li Y, Chen F, Putt M, Koo YK, Madaio M, Cambier JC, Cohen PL, Eisenberg RA (September 2008). "B cell depletion with anti-CD79 mAbs ameliorates autoimmune disease in MRL/lpr mice". Journal of Immunology. 181 (5): 2961–72. PMC 2865432. PMID 18713966.
  8. Hardy IR, Anceriz N, Rousseau F, Seefeldt MB, Hatterer E, Irla M, Buatois V, Chatel LE, Getahun A, Fletcher A, Cons L, Pontini G, Hertzberg NA, Magistrelli G, Malinge P, Smith MJ, Reith W, Kosco-Vilbois MH, Ferlin WG, Cambier JC (February 2014). "Anti-CD79 antibody induces B cell anergy that protects against autoimmunity". Journal of Immunology. 192 (4): 1641–50. doi:10.4049/jimmunol.1302672. PMC 3941979. PMID 24442438.

External links