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Updated: Aug 19, 2026

Induction and Assessment of Class Switch Recombination in Purified Murine B Cells
Published on: August 14, 2010
Inducing specific reactivity against B cells in mice by immunizing with an Fc fusion protein containing self-Igbeta
Jim J C Sheu1, Janice Huang, Tse W Chang
1Department of Life Science, National Tsing Hua University, Hsinchu 300, Taiwan.
A recombinant chimeric fusion protein, muIgbeta-hugamma4.Fc, composed of the extracellular domain of mouse Igbeta (CD79b) and the CH2-CH3 domains of human IgGgamma4.Fc (hugamma4.Fc), linked via an immunologically inert flexible peptide, was prepared. The fusion protein was evaluated for its ability to induce specific auto-reactive immune response against Igbeta and to modulate B cell activity in Balb/c mice. Upon immunization with muIgbeta-hugamma4.Fc, mice developed immunoglobulin (IgG) against self-Igbeta, which could bind to the cells of a mouse B cell line expressing Igbeta on the cell surface. The proportion of B cells in mononuclear cells in the peripheral blood (PBMC) of treated mice decreased as compared to that of mice immunized with hugamma4.Fc without the Igbeta component. Furthermore, mice immunized against muIgbeta-hugamma4.Fc displayed a reduced antibody response against an irrelevant antigen. The implications of employing the present approach in developing a therapeutic strategy for regulating B cell activity has been discussed.
A recombinant chimeric fusion protein, muIgbeta-hugamma4.Fc, composed of the extracellular domain of mouse Igbeta (CD79b) and the CH2-CH3 domains of human IgGgamma4.Fc (hugamma4.Fc), linked via an immunologically inert flexible peptide, was prepared. The fusion protein was evaluated for its ability to induce specific auto-reactive immune response against Igbeta and to modulate B cell activity in Balb/c mice. Upon immunization with muIgbeta-hugamma4.Fc, mice developed immunoglobulin (IgG) against self-Igbeta, which could bind to the cells of a mouse B cell line expressing Igbeta on the cell surface. The proportion of B cells in mononuclear cells in the peripheral blood (PBMC) of treated mice decreased as compared to that of mice immunized with hugamma4.Fc without the Igbeta component. Furthermore, mice immunized against muIgbeta-hugamma4.Fc displayed a reduced antibody response against an irrelevant antigen. The implications of employing the present approach in developing a therapeutic strategy for regulating B cell activity has been discussed.
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