CD79

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 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
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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
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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.