BCR-crosslinking induces a transcription of protein phosphatase component G5PR that is required for mature B-cell survival
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Updated: Aug 14, 2026

In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells
Published on: January 20, 2019
Faisal Mahmudul Huq Ronny1, Hideya Igarashi, Nobuo Sakaguchi
1Department of Immunology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1, Honjo, Kumamoto 860-8556, Japan.
Abstract:
BCR-crosslinking triggers activation-induced cell death (AICD) selectively in the restricted stage of B-cell differentiation. We examined the transcription of a protein phosphatase subunit G5PR in immature and mature B-cells, because absence of this factor augmented cell sensitivity to AICD, associated with increased activation of JNK and Bim. BCR-crosslinking-induced G5pr transcription in AICD-resistant mature splenic IgM(lo)IgD(hi) B-cells but not in AICD susceptible immature IgM(hi)IgD(lo) B-cells. Thus, G5pr induction correlated with the prevention of AICD; High in mature splenic CD23(hi) B-cells but low in immature B-cells of neonatal mice, sub-lethally irradiated mice, or xid mice. Lack of G5pr upregulation was associated with the prolonged activation of JNK. The G5pr cDNA transfection protected an immature B-cell line WEHI-231 from BCR-mediated AICD. The differential expression of G5PR might be responsible for the antigen-dependent selection of B-cells.
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