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International Immunology, Vol. 11, No. 6, 915-923, June 1999
© 1999 Japanese Society for Immunology

IgG1 production by sIgD+ splenic B cells and peritoneal B-1 cells in response to IL-5 and CD38 ligation

Tokutaro Yasue, Masashi Baba, Shigeo Mori1, Chieko Mizoguchi, Shoji Uehara and Kiyoshi Takatsu

Departments of Immunology and
1 Pathology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.

Correspondence to: K. Takatsu

CD38 ligation on mouse B cells by CS/2, an anti-mouse CD38 mAb, induces proliferation, IL-5 receptor {alpha} chain expression and tyrosine phosphorylation of Bruton's tyrosine kinase. Furthermore, stimulation of splenic B cells with IL-5 together with CS/2 induces Blimp-1 expression and differentiation into Ig-producing cells. Here we examined the role of IL-5 in IgG1 and IgA production by B cells isolated from the spleen and peritoneal cavity. CD38 recognized by CS/2 was expressed in the follicular mantle B cells surrounding the germinal center, sIgD+ splenic B cells and peritoneal B cells. IL-5 induced IgG1 production in splenic sIgD+ B cells stimulated with CS/2, while it was ineffective to induce IgA production. Among the various cytokines tested, only IL-5 had a synergistic effect on IgG1 production with CS/2. IL-5 could induce the generation of Sµ–S{gamma}1 reciprocal recombination DNA products in CS/2-stimulated B cells. IL-4 was ineffective to induce either µ–{gamma}1 switch recombination or IgG1 secretion with CS/2, demonstrating that IL-5 promotes both µ–{gamma}1 switch recombination and IgG1 secretion in an IL-4-independent manner. The peritoneal B-2 cells exhibited both IgG1 and IgA production in response to IL-5 plus CS/2, while B-1 cells produced IgG1. These results imply that the pattern of differentiation to Ig-producing cells seen with peritoneal B cells is not identical to the pattern seen with splenic B cells and that peritoneal B-2 cells contain precursors of IgA-producing cells responding to IL-5 plus CS/2.

Keywords: B-1 cells, CD38, IgA, IgG1, IL-5, switch recombination

The first two authors contributed equally to this work

Transmitting editor: M. Miyasaka


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