GALLIUM-ARSENIDE SELECTIVELY SUPPRESSES ANTIGEN-PROCESSING BY SPLENICMACROPHAGES FOR CD4(-CELL ACTIVATION() T)

Gallium arsenide (GaAs) is an intermetallic compound used in the elect ronics industry as a semiconductor. Acute exposure of animals to GaAs suppresses various immune functions. We investigated the effects of Ga As on immunocompetency with emphasis on macrophages. Mice were given 1 2.5 to 200 mg/kg GaAs i.p., and immune parameters were examined 1 or 5 days later. Chemically exposed mice did not display alteration in spl enic cellular composition. Despite this, primary in vitro humoral resp onse to sheep red blood cells by GaAs-exposed mice was inhibited in a dose-dependent manner. The ability of 5-day vehicle- or 200 mg/kg GaAs -exposed splenic macrophages to induce interleukin-2 production by ant igen-specific CD4(+) helper T cell hybridomas stimulated with soluble protein antigens was assessed. GaAs-exposed macrophages were less comp etent in eliciting T cell responses to pigeon cytochrome c and pork in sulin than vehicle-exposed cells. However, GaAs-exposed macrophages ac tivated hen egg lysozyme- and chicken ovalbumin-specific T cells as ef ficiently as vehicle control cells. Also, suppressed processing of cyt ochrome c was not observed after a 1-day exposure. Chemical exposure d id not alter the expression of major histocompatibility complex class II molecules on the macrophages or their activation of T cells by pept ides, which do not require processing. Therefore, GaAs causes a time- and antigen-dependent defect in antigen processing that is essential f or CD4(+) T cell stimulation by splenic macrophages.