Abstract
The Cd79a (Ig-a/mb-1) and CD79b (Ig-b/B29) molecules form a membrane heterodimer that is non-covalently associated with surface membrane immunoglobulin and is the major signaling component of B cell antigen receptor complex. The CD79a and CD79b also involve in the expression and internalization of surface immunoglobulin. We report three novel transcripts, which are generating by alternative splicing, of mouse CD79a from splenic cells of both BALB/c and C57BL/6 mice. These variant transcripts are predicted to enconde truncated forms of CD79a that result in the deletion of different portions of the extracellular domain. Their presence and relative amount have been performed by an RNAse protection assay. The definition of these variant transcripts provides a basis for continuing effort to define variant protein products of CD79a and examine their role in B cell physiology. In addition, the DNA sequence of CD79a from our present study showed one base insertion and followed one base deletion to the one reported by other group, resulting a sex amino acid change and one less cysteine in the extracellular portion of mouse CD79a.We are also investigating the possibility of inducing immune response against an autologous B cell-specific antigen, CD79b (Igb), a component of the B cell receptor complex, and the effects of this specific autoimmune activity, if generated, on B cells and the immune system. For inducing such an autoimmune response in BALB/c mice, we prepared a recombinant antigen, which is composed of the extracellular portion of mouse transmembrane Igb protein and the CH2 and CH3 domains of human g4 immunoglobulin chain. The foreign human g4 component is included to provide antigenic determinants for helper T cells. The dimeric Igb-Fc fusion protein was produced by expressing the corresponding composite gene in CHO cells. After BALB/c mice were immunized with the fusion protein in incomplete Freund’s adjuvant, the mice developed IgG to the extracellular portion of mouse Igb protein, as determined by ELISA. The sera from these immunized mice could specifically stain a mouse B cell line, BAL17, which expresses Igb on cell surface, as analyzed by flow cytometry. Furthermore, in mice immunized with Igb-Fc, who produced autoantibodies against Igb, the embers of total B cells in blood decreased significantly, as compared to those of mice immunized with human IgG without the Igb. The levels of total IgG in the blood of the immunized mice also decreased about 30% as compared to those of control mice. After that, the immunized mice then were re-immunized twice. The B-cell ration of some mice decreased from 50% to as low as 7%. The results have shown that specific autoimmune antibodies against Igb can be actively induced by immunizing with Igb coupled with a foreign antigen and that such autoantibody response can affect the levels of B cells and their activities.