Roles of CD4+and CD8+T cells in adjuvant activity of diesel exhaust particles in mice

Through an imbalance in Th1 and Th2 cytokine profiles, diesel exhaust parti cles (DEP) are thought to induce Th2-dominated IgE and IgG1 production. How ever, the roles of CD4+ and CD8+ T-cell subtypes in the increased immune re sponses to antigen in mice exposed to DEP are unclear. In the present study , we investigated whether treatment with anti-CD4 or anti-CD8 mAb abrogated the adjuvant activity of DEP. On day -1 and day 1, each group of mice was injected intraperitoneally with anti-CD4, anti-CD8, or rat IgG (vehicle). O n day 0, the mice were immunized with ovalbumin (OVA) or OVA plus DEP. Afte r 3 weeks, each mouse was boosted with in mug of OVA alone. On day 7 after the first injection with OVA+DEP or OVA alone, the numbers of total, IA+, C D80+/IA+ and CD86+/IA+ cells in peritoneal exudate cells (PEC) were higher in OVA+DEP-immunized mice than in OVA-immunized mice. Depletion of CD8+ cel ls resulted in a modulation of the production of granulocyte-macrophage col ony-stimulating factor, IL-12 and PGE(2) in peritoneal exudate fluid from O VA+DEP-immunized mice. On day 28, DEP injection markedly increased IL-4 pro duction in the culture supernatants of spleen cells from CD4+ or CD8+-deple ted mice. Depletion of CD8+ cells in OVA+DEP-immunized mice resulted in a d ecrease in IFN-gamma production compared with that in OVA-immunized mice. A djuvant activity of DEP was observed in anti-OVA IgE, anti-OVA IgG1, anti-O VA IgG3, and total IgE production. Depletion of CD4+ T cells abrogated the adjuvant effect of DEP on anti-OVA IgE, and anti-OVA IgG1 production in pla sma. However, depletion of CD8+ T cell inhibited the upregulated anti-OVA I gG3 production. These findings suggest that DEP injection may affect not on ly the function of CD4+ cells but also that of CD8+ T-cell subsets to modul ate the synthesis of proinflammatory cytokine in PEC and type-1 and type-2 cytokine production in spleens. Copyright (C) 2001 S. Karger AG, Basel.