IL-10 stimulates murine antigen-driven antibody responses in vitro by regulating helper cell subset participation.

The effects of IL-10 on in vitro antigen-driven murine antibody responses and helper cell IL-4 and IFN-gamma secretory capacity were investigated. Low antigen concentrations stimulated high responses in all antibody isotypes examined; IgD was not assayed. Under these conditions, exogenous IL-10 minimally potentiated synthesis of antigen-specific IgM, IgG1, IgG2a, IgG2b, IgG3, and IgA, but inhibited antigen-specific IgE secretion. High antigen levels stimulated antigen-specific IgM, IgG2a, and IgG2b responses, but inhibited synthesis of all other isotypes. In high antigen cultures, IL-10 augmented secretion of antigen-specific antibody in all isotypes except IgE. Essentially all of the antibody produced in the presence of high or low antigen concentrations was antigen-specific. Exogenous IL-10 substantially stimulated production of antigen-nonspecific antibody in all isotypes except IgG3. IL-10 allowed for greater Ig+ cell yield; comparable numbers of CD4+ and CD8+ cells were observed in the presence or absence of IL-10 in culture. The stimulatory effects of IL-10 for in vitro antibody responses were observed during a limited period of time after in vivo antigen priming of the responding cell populations. In contrast, IL-10 inhibited IgE synthesis at all time points tested. Low concentrations of antigen maintained the in vitro capacity of helper cells to secrete IL-4, while high antigen concentrations did not. Exogenous IL-10 potentiated IL-4 secretory capacity in high antigen cultures. The capacity for IFN-gamma secretion was comparable in high and low antigen cultures and exogenous IL-10 significantly inhibited such capacity under both sets of conditions. We conclude that IL-10 is generally stimulatory for murine antibody responses in vitro, with the possible exception of antigen-specific IgE. Such stimulatory effects appear to reflect increased activity of type 2 helper cells with concurrent decrease in type 1 helper cell activity.