Cd79a, also known as Igα, is a crucial signaling component of the preB cell receptor (preBCR) [1]. It is essential for B cell development as its successful expression marks the transition from pro-B to pre-B cells [4]. The BCR, composed of surface-bound Ig and a heterodimeric signaling unit of CD79A and CD79B, initiates important signals for B cell development, function, and tonic survival signaling. CD79A and CD79B are required for surface IgM expression in human B cells [3].

In a Cd79a-Cre;Tsc1ff mouse model (Cd79a-Tsc1 KO), Cre-mediated Tsc1 depletion driven by the Cd79a promoter activated mTORC1 exclusively along the distal nephron from embryonic day 16. This led to cyst formation in the distal nephron, suggesting that mTORC1 overactivation in developing distal tubules, mediated by Cd79a, disrupts morphogenesis and is involved in polycystic kidney disease-like cystogenesis [2]. In pediatric B-cell precursor acute lymphoblastic leukemia, downregulation of Cd79a in murine xenograft models hampered leukemia cell engraftment, especially in the central nervous system, indicating its role in CNS-infiltration and engraftment [1].

In conclusion, Cd79a is vital for B cell development and plays a role in maintaining B cell fitness through BCR-related functions. Mouse models, such as the Cd79a-Tsc1 KO and murine xenograft models, have revealed its significance in diseases like polycystic kidney disease and B-cell precursor acute lymphoblastic leukemia, providing insights into disease mechanisms and potential therapeutic targets.