Biology: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 |
Introduction
| 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 |
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 (also known as Igα and Igβ); 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]
Function
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
- ↑ 1.0 1.1 "CD79: a review". Applied Immunohistochemistry & Molecular Morphology 9 (2): 97–106. June 2001. doi:10.1097/00022744-200106000-00001. PMID 11396639.
- ↑ "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. June 1992. doi:10.1084/jem.175.6.1511. PMID 1375264.
- ↑ "Interplay between the human TCR/CD3 epsilon and the B-cell antigen receptor associated Ig-beta (B29)". Immunology Letters 44 (2–3): 97–103. January 1995. doi:10.1016/0165-2478(94)00199-2. PMID 7541024.
- ↑ Naeim, Faramarz; Rao, P. Nagesh; Song, Sophie X.; Grody, Wayne W. (2013). "Principles of Immunophenotyping". Atlas of Hematopathology. pp. 25–46. doi:10.1016/b978-0-12-385183-3.00002-4. ISBN 9780123851833.
- ↑ 5.0 5.1 "B-cells and their targeting in rheumatoid arthritis--current concepts and future perspectives". Autoimmunity Reviews 11 (1): 28–34. November 2011. doi:10.1016/j.autrev.2011.06.010. PMID 21777703.
- ↑ "Chronic active B-cell-receptor signalling in diffuse large B-cell lymphoma" (in En). Nature 463 (7277): 88–92. January 2010. doi:10.1038/nature08638. PMID 20054396. Bibcode: 2010Natur.463...88D.
- ↑ "B cell depletion with anti-CD79 mAbs ameliorates autoimmune disease in MRL/lpr mice". Journal of Immunology 181 (5): 2961–72. September 2008. doi:10.4049/jimmunol.181.5.2961. PMID 18713966.
- ↑ "Anti-CD79 antibody induces B cell anergy that protects against autoimmunity". Journal of Immunology 192 (4): 1641–50. February 2014. doi:10.4049/jimmunol.1302672. PMID 24442438.
External links
- CD79+Antigens at the US National Library of Medicine Medical Subject Headings (MeSH)
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