Swiss mice were immunized with various antigens: polyvinylpyrrolidone (PVP), human serum transferrin (HST), bovine serum albumin (BSA) or tetanus toxoid (TT). Fifteen days after the last injection of antigen, the mice were infected with Plasmodium chabaudi AJ. Two weeks after the beginning of malarial infection, parasitaemia became latent and total gammaglobulin levels, as well as IgG and IgM levels, were significantly increased. At that period the antigen-binding capacity (ABC) and the total antigen-binding Sites (Abt) were determined for PVP, HST and BSA. It appeared that the ABC and Abt of anti-HST or anti-BSA antibodies were lower than those of corresponding uninfected controls. With regard to anti-PVP antibodies, only the Abt was modified after infection, but not the ABC. The evolution of anti-TT Ab levels determined by a solid-phase assay with 125I-TT was as above with a marked decrease on and after the 4th week of infection. Injection of low-density lipoproteins (LDL) from day-9-infected mice to TT-immunized mice significantly reduced anti-TT antibody levels. At similar doses, LDL from normal mice did not induce an inhibitory effect. At mouse-equivalent-dose, LDL from infected mice revealed an inhibitory effect compared to LDL from uninfected controls. Our results suggest that LDL from P. chabaudi-infected mice can exert an immunoregulatory role and thus could explain part of the immune impairment observed during the infective process. Moreover, from the present data it might be postulated that the hypergammaglobulinaemia of P. chabaudi infection does not result from a parasite-potentiating effect on a pre-existing antibody response.