Defective resistance to Plasmodium yoelii in CBA/N mice.
The role of B lymphocytes in resistance to malaria was studied in defective and normal F1 mice derived from CBA/N mice, a strain with an X-linked B cell defect. When infected with normally nonlethal Plasmodium yoelii, immune defective F1 male mice had higher parasitemias and more prolonged infections than normal F1 mice, as well as a 50% mortality rate. Before infection the plasma levels of IgM and IgG were lower in defective F1 males than normal F1 mice. The polyclonal IgM and IgG responses of infected abnormal F1 mice were delayed and lower in absolute magnitude than those of normal F1 mice. Furthermore, specific IgM and IgG anti-plasmodial antibody titers, as determined by radioimmunoassay, were depressed on day 12 in the defective F1 males. Although IgG titers approached those of the normal F1 mice on day 19, defective F1 male IgM titers remained depressed. These data demonstrate that an X-linked gene that affects B cell function influences malarial resistance in mice, presumably via a decreased specific IgM response, and the slow development of a specific IgG response to P. yoelii infection.
D000818:Animals; D000906:Antibodies / Q000276:immunology; D005260:Female; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D007153:Immunologic Deficiency Syndromes / Q000235:genetics; D008288:Malaria / Q000235:genetics / Q000517:prevention & control*; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA; D010961:Plasmodium / Q000276:immunology
D000906:Antibodies; D007074:Immunoglobulin G; D007075:Immunoglobulin M