Trypanosoma musculi infection in B-cell-deficient mice.
The course of infection with Trypanosoma musculi was assessed in mice deprived of B-lymphocytes by administration, from birth, of rabbit antiserum to mouse immunoglobulin M (IgM). Initial control of parasitemia leading to the first crisis and establishment of the plateau phase was unaffected by lack of B-lymphocyte function, although multiplicative forms persisted throughout the infection in anti-IgM-treated mice, instead of disappearing after the first crisis as in intact mice. Elimination of trypanosomes after the second crisis was not observed in anti-IgM-treated mice, which maintained high numbers of parasites in the blood and peritoneal cavity, resulting in some mortality. A temporary reduction in parasitemia was achieved in anti-IgM-treated mice by transfusion of immune plasma. Immunodepression, as measured by splenic mitogen responsiveness, and splenomegaly were both observed in anti-IgM-treated as well as in intact mice, indicating that these features of murine trypanosomiasis are independent of B-lymphocyte function. Since in T. musculi infection parasitemia can be controlled initially but not eliminated in mice lacking B-cell function, the only crucial protection provided by antibody would appear to be in curing the infection after the second crisis.
D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology*; D001769:Blood / Q000469:parasitology; D005260:Female; D007117:Immunization, Secondary; D007074:Immunoglobulin G / Q000096:biosynthesis; D007075:Immunoglobulin M / Q000096:biosynthesis / Q000276:immunology; D051379:Mice; D008934:Mitogens / Q000494:pharmacology; D013154:Spleen / Q000166:cytology; D013601:T-Lymphocytes / Q000276:immunology; D014345:Trypanosoma / Q000302:isolation & purification; D014352:Trypanosomiasis / Q000276:immunology* / Q000469:parasitology / Q000628:therapy
D000888:Antibodies, Anti-Idiotypic; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D008934:Mitogens