CD79

CD79a molecule, immunoglobulin-associated alpha
Identifiers
Symbol	CD79A
Alt. symbols	IG-alpha
NCBI gene	973
HGNC	1698
OMIM	112205
RefSeq	NM_001783
UniProt	P11912
Other data
Locus	Chr. 19 q13.2
Search for Structures Swiss-model Domains InterPro

CD79b molecule, immunoglobulin-associated beta
Identifiers
Symbol	CD79B
Alt. symbols	IG-beta
NCBI gene	974
HGNC	1699
OMIM	147245
RefSeq	NM_021602
UniProt	P40259
Other data
Locus	Chr. 17 q23
Search for Structures Swiss-model Domains InterPro

The CD79 receptor complex, also known as CD79A:CD79B or Igα:Igβ, is a heterodimeric signaling component of the B-cell receptor (BCR) complex. This transmembrane heterodimer consists of the B-cell antigen receptor complex-associated protein alpha chain (CD79A/Igα) and the B-cell antigen receptor complex-associated protein beta chain (CD79B/Igβ). The CD79 complex is expressed almost exclusively on B cells and B-cell neoplasms, making it valuable for differential diagnosis of B-cell malignancies from T-cell or myeloid neoplasms.^[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]

Utilization

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.

References

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, et al. (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): 1511–1519. 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 (2013). "Principles of Immunophenotyping". Atlas of Hematopathology. pp. 25–46. doi:10.1016/b978-0-12-385183-3.00002-4. ISBN 978-0-12-385183-3.
5. Nakken B, Munthe LA, Konttinen YT, Sandberg AK, Szekanecz Z, Alex P, et al. (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. hdl:2437/126828. PMID 21777703.
6. Davis RE, Ngo VN, Lenz G, Tolar P, Young RM, Romesser PB, et al. (January 2010). "Chronic active B-cell-receptor signalling in diffuse large B-cell lymphoma". Nature. 463 (7277): 88–92. Bibcode:2010Natur.463...88D. doi:10.1038/nature08638. PMC 2845535. PMID 20054396.
7. Li Y, Chen F, Putt M, Koo YK, Madaio M, Cambier JC, et al. (September 2008). "B cell depletion with anti-CD79 mAbs ameliorates autoimmune disease in MRL/lpr mice". Journal of Immunology. 181 (5). Baltimore: 2961–2972. doi:10.4049/jimmunol.181.5.2961. PMC 2865432. PMID 18713966.
8. Hardy IR, Anceriz N, Rousseau F, Seefeldt MB, Hatterer E, Irla M, et al. (February 2014). "Anti-CD79 antibody induces B cell anergy that protects against autoimmunity". Journal of Immunology. 192 (4). Baltimore: 1641–1650. doi:10.4049/jimmunol.1302672. PMC 3941979. PMID 24442438.

External links

• CD79+Antigens at the U.S. National Library of Medicine Medical Subject Headings (MeSH)