Abstract
Swiss Webster mice were exposed to excess dietary aluminum (Al) (1000 μg Al/g diet, Al as Al lactate) from conception to 6 months of age. Splenic lymphocytes (106 per culture) were incubated for 24 hrs with concanavalin A (5 μg/ml). Concentrations of interleukin-2, interferon-γ and tumor necrosis factor-a, as measured in supernatants via ELISA with monoclonal antibodies, were depressed in spleen cells from aluminum treated mice relative to controls. Experiments using the flourescence activated cell sorter demonstrated a shift in T-cell populations from treated mice with a deficiency of CD4+ cells. These findings suggest a deficit in immune effector cell function after long term in vivo aluminum exposure.