The transcriptional programme of antibody class switching involves the repressor Bach2

Akihiko Muto, Satoshi Tashiro, Osamu Nakajima, Hideto Hoshino, Satoru Takahashi, Eiichirou Sakoda, Dai Ikebe, Masayuki Yamamoto and Kazuhiko Igarashi ()
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Akihiko Muto: Hiroshima University Graduate School of Biomedical Sciences
Satoshi Tashiro: Hiroshima University Graduate School of Biomedical Sciences
Osamu Nakajima: Yamagata University
Hideto Hoshino: University of Tsukuba
Satoru Takahashi: University of Tsukuba
Eiichirou Sakoda: Hiroshima University Graduate School of Biomedical Sciences
Dai Ikebe: Hiroshima University Graduate School of Biomedical Sciences
Masayuki Yamamoto: University of Tsukuba
Kazuhiko Igarashi: Hiroshima University Graduate School of Biomedical Sciences

Nature, 2004, vol. 429, issue 6991, 566-571

Abstract: Abstract Activated B cells differentiate to plasma cells to secrete IgM or, after undergoing class switch recombination (CSR), to secrete other classes of immunoglobulins1,2,3,4. Diversification of antibody function by CSR is important for humoral immunity. However, it remains unclear how the decision for the bifurcation is made. Bach2 is a B-cell-specific transcription repressor interacting with the small Maf proteins whose expression is high only before the plasma cell stage5,6,7. Here we show that Bach2 is critical for CSR and somatic hypermutation (SHM)2,4,8 of immunoglobulin genes. Genetic ablation of Bach2 in mice revealed that Bach2 was required for both T-cell-independent and T-cell-dependent IgG responses and SHM. When stimulated in vitro, Bach2-deficient B cells produced IgM, as did wild-type cells, and abundantly expressed Blimp-1 (refs 9, 10) and XBP-1 (ref. 11), critical regulators of the plasmacytic differentiation12, indicating that Bach2 was not required for the plasmacytic differentiation itself. However, they failed to undergo efficient CSR. These findings define Bach2 as a key regulator of antibody response and provide an insight into the orchestration of CSR and SHM during plasma cell differentiation.

Date: 2004
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DOI: 10.1038/nature02596

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