Induction of T helper 2 responses against human apolipoprotein B100 does not affect atherosclerosis in ApoE−/− mice

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Immune responses against LDL antigens have been found to play an important modulatory role in atherosclerosis. Immunization with homologous oxidized LDL, as well as human apolipoprotein B100 (ApoB)-derived peptides, inhibits atherosclerosis in hypercholesterolaemic animal models of atherosclerosis. However, the role of antigen-specific T helper 2 (Th2) responses in atherosclerosis remains to be fully clarified.

Methods and results

ApoE−/− mice on high-fat diet were immunized with human ApoB using Alum as an adjuvant at 12, 14, and 16 weeks of age. Alum-injected and non-treated mice were used as controls. At 17 weeks of age, a matrigel plug containing ApoB was placed subcutaneously and T-cell infiltration into the plug as well as the development of aortic root atherosclerotic lesions were analysed after an additional 7 days. Immunization with ApoB resulted in four-fold increased accumulation of effector T cells in ApoB-containing matrigel when compared with control groups. The levels of the Th2 cytokines IL-4, IL-5, and IL-10 were also increased in ApoB-containing matrigel plugs. Moreover, the levels of Th2-associated IgG1 against human and also mouse LDL were increased in the plasma of ApoB-immunized mice. In spite of the induction of a Th2 response partially reacting also with the endogenous LDL, there was no difference in atherosclerosis when compared with the Alum group.


This study describes a novel model to study antigen-specific T-cell responses in vivo in mouse models of atherosclerosis. The results suggest that activation of Th2 immunity does not mediate the protective effect of immunization with LDL antigens described previously.

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