Experimental malaria in the CBA/N mouse.
CBA/N mice carry an X-linked, recessive gene, which results in the absence of a B cell subset, and is expressed primarily as an inability to respond to a certain class of thymus-independent antigens. We have examined the responses of these mice to the malaria parasite Plasmodium yoelii and found that primary infections induced by this parasite are more severe and last longer in mice with X-linked defect than in normal controls. The decreased resistance of the defective mice is associated with a striking deficiency in their IgM antibody response. After recovery from a primary infection, defective mice resist reinfection with the homologous parasite as well as normal mice. Although as resistant as normal controls, B cells from defective mice transfer considerably less immunity to naive recipients than B cells from normal animals. Hence, two modes of thymus-dependent protective immunity may contribute to the host response to P. yoelii. Control of an acute primary infection appears to involve a thymus-dependent antibody response that CBA/N mice are deficient in. Resistance to reinfection may be mediated primarily by a different mechanism.
D000818:Animals; D000917:Antibody Formation; D001323:Autoantibodies / Q000096:biosynthesis; D004912:Erythrocytes / Q000276:immunology; D005260:Female; D005455:Fluorescent Antibody Technique; D007116:Immunization, Passive; D008288:Malaria / Q000097:blood / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D010961:Plasmodium / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D014960:X Chromosome
D001323:Autoantibodies