Literature DB >> 17532053

Bcl6 is required for the IL-4-mediated rescue of the B cells from apoptosis induced by IL-21.

Nobuhide Tsuruoka1, Masafumi Arima, Eggi Arguni, Thoru Saito, Daisuke Kitayama, Akemi Sakamoto, Masahiko Hatano, Takeshi Tokuhisa.   

Abstract

IL-21 has a pro-apoptotic effect on freshly isolated B cells stimulated with LPS, and also induces Bcl6 expression in the activated B cells. However, a role for Bcl6 in the activated B cells is not known. When naive B cells from Bcl6-deficient mice were stimulated with LPS plus IL-21, those B cells died by apoptosis as wild-type B cells. Co-stimulation of those B cells with IL-4 partially rescued the wild-type B cells but not the Bcl6-deficient B cells from the IL-21-induced apoptosis. Bcl-2 was not up-regulated in both B cells stimulated with LPS plus IL-21 and IL-4. Bcl-X(L) and Bax were up-regulated in both B cells stimulated with LPS plus IL-4, and the co-stimulation with IL-21 did not modulate these up-regulations in wild-type B cells. However, the co-stimulation clearly suppressed the Bcl-X(L) up-regulation but not the Bax up-regulation in Bcl6-deficient B cells. Thus, Bcl6 is required for maintaining the Bcl-X(L) up-regulation in B cells stimulated with LPS plus IL-21 and IL-4, and the up-regulation may partially rescue the B cells from apoptosis induced by IL-21.

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Year:  2007        PMID: 17532053     DOI: 10.1016/j.imlet.2007.04.009

Source DB:  PubMed          Journal:  Immunol Lett        ISSN: 0165-2478            Impact factor:   3.685


  3 in total

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3.  The Human Blood Metabolome-Transcriptome Interface.

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Journal:  PLoS Genet       Date:  2015-06-18       Impact factor: 5.917

  3 in total

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