Langhorne J, Asofsky R
Max Planck Institute of Immunobiology, Freiburg, Federal Republic of Germany.
Immunobiology. 1987 Aug;174(4-5):432-43. doi: 10.1016/S0171-2985(87)80016-5.
The influence of an infection with P. chabaudi adami on the isotypic distribution of the in vivo antibody response to SRBC was investigated. Previous experiments suggested that the IgG1 isotype was poorly represented in the antibody response to plasmodial antigens and in the non-specific B cell response which accompanies an infection with P. chabaudi. The experiments described here indicated that although the magnitude of the total primary or secondary in vivo PFC response to SRBC was relatively unaffected by infection, the SRBC-specific IgG1 PFC response was depressed. Maximum depression of the IgG1 component of the response was observed when the priming dose of SRBC was administered at the same time as or after infection with P. chabaudi organisms. Coincident with the depression in the IgG1 response in infected mice was a corresponding increase in the SRBC-specific IgM response. The IgG1 depression was not a consequence of different kinetics of the generation of an IgG1 response, since at all times measured, the IgG1-PFC response was lower. In addition, the depressed IgG1 responses occurred only during a viable infection and could not be induced by inoculation of large amounts of irradiated erythrocytic stages of the parasite. These data suggest therefore, that there is a selective depression of IgG1 antibodies (but not those of other isotypes) regardless of antigenic specificity as a result of infection of C57BL/6 mice with P. chabaudi adami.