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Inbred mice infected with Plasmodium yoelii differ in their antimalarial immunoglobulin isotype response
Author(s) -
TAYLOR DIANE W.,
PACHECO ELAINE,
EVANS CHARLES B.,
ASOFSKY RICHARD
Publication year - 1988
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.1988.tb00201.x
Subject(s) - plasmodium yoelii , isotype , biology , antibody , immunology , virology , malaria , immunoglobulin d , immunoglobulin g , humoral immunity , plasmodium falciparum , parasitemia , b cell , monoclonal antibody
Summary Antibodies are known to be important in mediating malarial immunity, but the influence of the various immunoglobulin isotypes on parasite elimination is unclear. The purpose of this study was to provide basic information on the induction of isotype expression in genetically different mice during primary malaria. Parasitaemias and the serum antimalarial IgM. Igd 1 , IgG 2 , IgG 3 and IgA antibody titres measured in a radioimmunoassay were followed in outbred and 11 inbred strains of mice infected with 17XNL Plasmodium yoelii. Severity of infection, as judged by length of infection, peak parasitaemias and death, was found to differ between the strains. All strains developed rapid IgM responses, but only 3/11 inbred strains produced significant antimalarial IgG 1 levels during primary infection. All strains produced an IgG 3 response, which developed slightly more quickly in strains with the least severe courses of malaria. A large variation in the IgG 3 response was noted between strains. In general, IgG 3 antibodies were the first IgG‐isotype to appear in serum. They were detected as early as day 8 in strains that developed mild infections but were not present until around day 20 in strains with the most severe cases of malaria. Only one strain produced detectable antimalarial IgA antibodies. These results show that different patterns of isotype expression are induced in inbred strains of mice during primary P. yoelii infection.