The ability of natural killer (NK) cells to secrete lymphokines confer
s upon them the potential to regulate cell types via mechanisms other
than direct cytotoxicity. During the past few years increasing evidenc
e has been accumulating to show that NK and B cells can interact produ
ctively. First, NK cells cocultured with B cells can induce them to in
itiate polyclonal Ig secretion. This help is mediated by a soluble fac
tor (or factors) that appears to be different from any known cytokine.
Second, preactivated B lymphocytes can induce NK cells to produce gre
ater amounts of IFN-gamma via an interaction that requires direct cell
contact. Third, in contrast to previous suggestions, NK cells do not
have the ability to kill primary B lymphocytes regardless of their sta
ge of differentiation. Evaluation of the in vivo relevance of these in
teractions revealed that activated NK cells can increase the IgG2a res
ponse to a specific protein antigen. Without activation, NK cells neit
her enhance nor inhibit B cell responses to antigens. The deviation of
the isotype distribution may allow increased NK cell specificity for
certain pathogens by enhancing antibody-dependent cytotoxicity.