OVAp priming increased the antibody response to β-galactosidase co-immunized with OVA DNA immunization. (A) Eight-week-old male C57BL/6 mice (n = 8) were primed with either OVAp or control INSp in complete Freund adjuvant. After 2 weeks, all mice were immunized by gene gun with pellets co-coated with plasmids encoding OVA and β-galactosidase. Two and 4 weeks later, IgG antibodies against β-galactosidase were higher (P = .001) in mice primed with OVAp, compared with those primed with the control INSp. After 12 weeks, β-galactosidase antibodies remained significantly higher (P = .01) in mice primed with OVAp compared to INSp. (B) Twelve days after OVAp priming, mice (n = 8) were treated with anti-CD8 antibody (0.5 mg 53.6.7 and 0.5 mg YTS169 intraperitoneally) or not. All mice were co-immunized with OVA and β-galactosidase DNA 2 days later. Three weeks after that, ELISA titers of anti–β-galactosidase responses were determined. (C) Pre-existing HSV-specific CTLs increase the antibody response to β-galactosidase when coexpressed with OVA-hsv. Eight-week-old male C57BL/6 mice were peptide primed with HSVp. After 3 weeks, mice were DNA immunized with pellets co-coated with β-galactosidase plasmid plus either OVA or OVA-hsv (in which the CTL epitope OVAp is substituted with HSVp). HSVp-primed mice had higher β-galactosidase antibodies (P = .01) after co-immunization with OVA-hsv compared with OVA. Mean and standard deviation are shown. ^*Statistical significance (P < .05).