The aging process is characterized by a progressive decline in the host's immune response profile. Moreover, optimal functioning of the immune system depends upon adequate levels of dietary zinc. In previous studies we have shown that supplemental zinc restores a large measure of immunocompetence to aging mice. In this proposal we endeavor to study possible mechanisms by which zinc activates antibody responses in immunodepressed, aged mice. Recent reports in the literature as well as preliminary data presented in this proposal suggest that interleukin 1 along with supplemental zinc constitute a minimum signal for the production of specific antibody by murine B cells. Further data suggest that the pathway by which B cells are activated involves cyclic AMP-dependent events. Using in vitro techniques we will culture purified populations of B lymphocytes from 24 month old mice. These cells will be activated with antigen along with interleukin 1 and will be supplemented with immunoenhancing, pharmacologic doses of zinc. Antibody responses will be monitored as will possible pathways of activation. Thus, we will examine the effects of I1-1 and zinc on cyclic AMP-dependent events, on interleukin 6 synthesis and on the induction of metal metallothionein mRNA synthesis.
