The MB1 gene, CD79a, is critical in the immune system. It encodes the Ig-α protein, a key component of the B cell antigen receptor complex. Ig-α non-covalently binds with surface immunoglobulin (Ig) and Ig-β, facilitating the expression function of the B cell antigen receptor. This gene is expressed early in B cell development, even before the V(D)J recombination occurs at the IgH locus. The CD79a gene is primarily expressed in lymphoid germinal centers and subgroups of peripheral immune cells, with notable cytoplasmic expression. CD79a and CD79b together form the B cell receptor (BCR) complex, which serves as an identity tag for B cells, recognizing specific antigens and initiating humoral immune responses. Mutations in the CD79a gene can lead to various immunodeficiencies, including X-linked agammaglobulinemia, characterized by a lack of mature B cells and antibodies. Moreover, CD79a is expressed in some malignant B cell tumors, making it a potential target for diagnosis and treatment.

Mb1-iCre mice were generated by integrating a codon-optimized Cre recombinase gene (iCre) expression cassette, which has higher recombination activity, into the endogenous Cd79a gene in the mouse, driving its specific expression. This strategy disrupts the expression of the mouse endogenous Cd79a gene. When bred with mice containing the loxP site-flanked sequence, Cre recombinase-mediated deletion of the flanked sequence is estimated to occur in the lymphoid B cells of the offspring mice, with a predicted high level of Cre recombinase activity in the early development of B cells.