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The Journal of Immunology, Vol 150, Issue 8 3215-3223, Copyright © 1993 by American Association of Immunologists
ARTICLES |
LM Pecanha, CM Snapper, A Lees, H Yamaguchi and JJ Mond
Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814-4799.
Lymphokines play a key role in T cell-independent (TI) Ag-induced responses. We recently showed that IL-10 potently inhibits Ig production stimulated by TI-2 Ag + IL-5. In view of our recent findings that the B cell activator can determine the effect lymphokines will have on Ig production and on isotype selection, we analyzed the effect of IL-10 on Ig production induced by other TI antigens and T cell- dependent Ag. These data demonstrate that IL-10 inhibited IL-5-induced Ig production stimulated by TI-1 and by TI-2 Ag, but had no effect on an in vitro T cell-dependent Ag-specific anti-SRBC-induced response or on a T cell-induced polyclonal response mediated by anti-CD3-activated T cell clones. IL-10 inhibited IgM, IgG1, IgG2a, and IgG3 secretion by B cells costimulated by LPS or anti-delta-dextran. IL-10 did not interfere with induction of class II MHC Ag expression or cell enlargement that was stimulated by LPS or anti-delta-dextran and had no detrimental effect on cell viability. IL-4 reversed the IL-10-mediated inhibition of IgG1 and IgM secretion stimulated by anti-delta-dextran or LPS-activated cells in the presence of IL-5. A 72 h, but not 24 h, exposure to IL-4 at initiation of culture with anti-delta-dextran + IL- 5 + IL-10 was necessary to reverse the IL-10-mediated inhibition of IgM secretion. Our data suggest that IL-10 can selectively inhibit TI Ag- induced responses when other T cell-derived stimulatory lymphokines are not present and further emphasize the specific role of the B cell activator in influencing the responsiveness of B cells to lymphokines.
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