Abstract
The effect of oral administration of lead, as Pb-acetate, via the drinking water on the murine delayed type hypersensitivity (DTH) response was investigated. The DTH response of BALB/c mice sensitized intraveneously with sheep red blood cells (SRBC) was found to be suppressed markedly in lead-intoxicated mice. Suppression of the DTH correlated with increasing blood Pb concentration. Suppression of the DTH response by Pb intoxication depended on the route of administration of the sensitizing antigen, as Pb intoxication did not impair the DTH reaction when mice were sensitized to SRBC via intraperitoneal injection. Since DTH reactions are regulated in large part by Th1 cells, these data establish an in vivo model system based on a rational route of Pb exposure in which to study further the modulation of Th1-mediated immune effector function by Pb.
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