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.
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.
^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. PMID7541024.
^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 9780123851833.
^ abNakken B, Munthe LA, Konttinen YT, Sandberg AK, Szekanecz Z, Alex P, Szodoray P (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. PMID21777703.
^Davis RE, Ngo VN, Lenz G, Tolar P, Young RM, Romesser PB, Kohlhammer H, Lamy L, Zhao H, Yang Y, Xu W, Shaffer AL, Wright G, Xiao W, Powell J, Jiang JK, Thomas CJ, Rosenwald A, Ott G, Muller-Hermelink HK, Gascoyne RD, Connors JM, Johnson NA, Rimsza LM, Campo E, Jaffe ES, Wilson WH, Delabie J, Smeland EB, Fisher RI, Braziel RM, Tubbs RR, Cook JR, Weisenburger DD, Chan WC, Pierce SK, Staudt LM (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. PMC2845535. PMID20054396.