Investigations into the role of NK cells in regulating Ab responses ha
ve yielded variable results, some suggesting that NK cells can down-re
gulate Ag-specific Ig production and others proposing an enhancing eff
ect. These apparently inconsistent findings may stem partially from th
e specificity of reagents used in purifying cell populations and/or th
e nature of the in vitro systems used to study these events. We chose
to investigate the ability of either resting or poly(I:C)-activated NK
cells to alter an in vivo Ab response in mice given a T-independent (
TNP-LPS) or T-dependent (TNP-keyhole limpet hemocyanin (KLH)) Ag. By u
sing a more specific Ab, anti-NK-1.1, to deplete NK cells, we were abl
e to clearly show that resting, endogenous NK cells do not affect eith
er type of response, as measured by serum Ag-specific Ig levels quanti
tated by isotype-specific ELISA. In contrast, activation of NK cells b
y poly(I:C) increased Ag-specific IgC2a as well as IgG1 levels. Intere
stingly, only the effect on IgG2a production is reversible by depletio
n of NK cells.