Cytokine production by spleen cells from mice with ovalbumin-specific, IgE-selective unresponsiveness induced by ovalbumin-liposome conjugate

Abstract

ABSTRACT Ovalbumin coupled with liposomes (OVA–liposome) induced selective unresponsiveness of anti-OVA IgE antibody production in BALB/c mice, whereas OVA adsorbed with aluminum hydroxide (OVA–alum) induced a substantial amount of anti-OVA IgE antibody production. Ovalbumin–liposome and OVA–alum predominantly induced IgG 2a and IgG 1 anti-OVA production, respectively. These results suggest that OVA–liposome and OVA–alum induce type 1 and type 2T helper (Th) immune responses, respectively. To further investigate this issue, we examined the cytokine production induced by these two distinct adjuvants. Spleen cells taken from mice immunized with either OVA–liposome or OVA–alum were cultured in vitro with OVA and the cytokine production from each culture was analyzed. It was demonstrated that spleen cells from mice immunized with OVA–liposome produced more interferon (IFN)-γ than those immunized with OVA–alum and, furthermore, interleukin (IL)-4 was produced only by spleen cells from mice immunized with OVA–alum. These results favor the notion that OVA–liposome and OVA–alum induce Th1 and Th2 cytokines, respectively. Interestingly, the production of IL-2, a Th1 cytokine, was higher in the OVA–alum-immunized group and the production of IL-10, a Th2 cytokine, remained at low levels in both groups after primary immunization; levels of IL-10 increased in the OVA–liposome-immunized group after secondary immunization. These results do not agree with the above notion and, thus, suggest that it may be important to consider the balance between IFN-γ-producing cells and IL-4-producing cells rather than that between Th1 and Th2 cells for the regulation of IgE antibody production.