Contents

CD79

Introduction[edit]

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[edit]

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[edit]

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[edit]

External links[edit]

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