TheCD79receptorcomplex, also known asCD79A:CD79B orIgα:Igβ, is aheterodimericsignaling component of theB-cell receptor (BCR) complex. Thistransmembrane heterodimer consists of theB-cell antigen receptor complex-associated protein alpha chain (CD79A/Igα) and theB-cell antigen receptor complex-associated protein beta chain (CD79B/Igβ). The CD79 complex is expressed almost exclusively onB cells and B-cellneoplasms, making it valuable fordifferential diagnosis of B-cell malignancies from T-cell or myeloid neoplasms.^[1]

CD79a and CD79b are both members of theimmunoglobulin superfamily. Human CD79a is encoded by themb-1 gene that is located onchromosome 19, and CD79b is encoded by theB29 gene that located onchromosome 17.^[1][2] Both CD79 chains contain animmunoreceptor tyrosine-based activation motif (ITAM) in theirintracellular tails that they use to propagate a signal in a B cell, in a similar manner toCD3-generated signal transduction observed duringT cell receptor activation onT cells.^[3]

CD79 serves to be a pan-B cell marker for the detection of B-cellneoplasms. However,tumor cells in some cases of T-lymphoblasticleukemia/lymphoma and AML has shown to potentially react positively with CD79 monoclonal antibodies.^[4] In addition, both CD79 chains contain animmunoreceptor 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 forsystemic lupus erythematosus (SLE).^[5] CD79, expressed by B-cell and plasma cell precursors is a candidate that inducesapoptosis as well as inhibition ofB-cell receptor (BCR) activation and possibly depletion of ectopic germinal centers (GC).^[5] However, research on CD79 still remains very open.

Scientists identified mutations in the BCR coreceptor CD79A/B that lead to chronic activation of BCR signaling. Somatic mutations affecting the ITAM signaling modules ofCD79B andCD79A 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.

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

• Genes on human chromosome 19
• Genes on human chromosome 17
• Clusters of differentiation
• Protein complexes

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