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The Journal of Immunology, Vol 157, Issue 8 3323-3333, Copyright © 1996 by American Association of Immunologists

ARTICLES

IL-10 inhibits lipopolysaccharide-induced murine B cell proliferation and cross-linking of surface antigen receptors or ligation of CD40 restores the response

JF Marcelletti
LIDAK Pharmaceuticals, La Jolla, CA 92037, USA.

The effects of IL-10 on murine B cell proliferation in vitro were investigated. IL-10 inhibited LPS-induced B cell proliferation with an EC50 of approximately 500 pg/ml. IL-10-mediated inhibitory activity was not overtly associated with cytotoxicity or induction of apoptosis. The presence or the absence of T cells and mononuclear phagocytes did not affect the inhibitory activity of IL-10 on LPS-induced proliferation. LPS-stimulated, IL-10-exposed B cells progressed from G0 or from M to G1A of the cell cycle, but were inhibited from entry into subsequent phases. IL-10 had no discernible effect on B cell proliferation elicited with goat anti-mouse IgM plus IL-4. Moreover, cross-linking, but not mere ligation, of surface Ag receptors restored LPS-induced B cell proliferation in the presence of IL-10. The proliferative response to ligation of CD40 with anti-CD40 Abs was also not inhibited by IL-10, and as observed with goat anti-mouse IgM, the presence of such Abs in IL-10-containing B cell cultures allowed for the proliferative response to LPS. A variety of other Abs reactive with murine B cell surface markers were ineffective at modulating the response to IL-10. IL-1, IL- 2, IL-4, IL-5, IL-6, IFN-gamma, and TGF-beta were also ineffective in this regard. These observations suggest that IL-10 has a role in the suppression of inappropriate B cell proliferation, i.e., proliferation by B cells that have not effectively interacted with relevant Ag or CD40 ligand.


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