Spleen cell-mediated suppression of IgG production to a non-parasite antigen during chronic Trypanosoma cruzi infection in mice.
Splenic plaque-forming cell (PFC) responses to TNP-BGG (thymus-dependent) and TNP-Ficoll (thymus-independent) were measured during acute and chronic T. cruzi infections produced in C57BL/10 mice. The number of anti-TNP PFC to both antigens was suppressed as has been shown. Approximately 40% of untreated mice survived acute disease to enter chronic T. cruzi infection characterized by a decrease in parasitemia, a reduction in spleen size, a return to normal of the IgM responses to TNP-BGG and TNP-Ficoll, persistant polyclonal activation, and continued suppression of the IgG responses to TNP-BGG. Mice that were drug-treated during the acute disease had high survival rates and similar immune response patterns, ie., suppressed IgG PFC responses to TNP-BGG and normal IgM PFC responses to TNP-BGG and TNP-Ficoll. The selective suppression of the IgG response was transferred to nonirradiated syngeneic recipients by Thy-1.2-positive cells present in the spleens of chronically infected mice. These observations may be interpreted to suggest the persistence of nonspecific suppressor T cells during chronic T. cruzi infections.
D000818:Animals; D000921:Antibody-Producing Cells / Q000276:immunology; D000941:Antigens / Q000008:administration & dosage* / Q000276:immunology; D000961:Antilymphocyte Serum / Q000008:administration & dosage; D014355:Chagas Disease / Q000276:immunology* / Q000469:parasitology; D002908:Chronic Disease; D006462:Hemolytic Plaque Technique; D007074:Immunoglobulin G / Q000096:biosynthesis*; D008213:Lymphocyte Activation; D051379:Mice; D008810:Mice, Inbred C57BL; D013154:Spleen / Q000166:cytology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D014302:Trinitrobenzenesulfonic Acid / Q000008:administration & dosage / Q000276:immunology
D000941:Antigens; D000961:Antilymphocyte Serum; D007074:Immunoglobulin G; D014302:Trinitrobenzenesulfonic Acid