Trypanosomal surface coat variant antigen causes polyclonal lymphocyte activation.

Abstract

Variant antigen, the primary component of the surface coat of the salivarian trypanosome, when injected i.v. into mice at dosages encountered during acute infections, produced some of the immunopathogenic phenomena associated with acute African trypanosomiasis. Trypanosome-infected and variant antigen-treated mice had splenomegaly caused by proliferation of null cells, B and T lymphocytes, and macrophages. Splenic B lymphocytes were nonspecifically activated to produce antibodies to sheep erythrocytes (SE), to trinitrophenylated-SE, and to fluoresceinated-SE. This polyclonal activation apparently depleted antigen-reactive lymphocyte populations as indicated by a reduced SE-specific, plaque-forming cell response after immunization in vitro. As judged from the results of in vitro immunization and mitogen assays, injections of variant antigen did not induce nonspecific immunosuppression, which indicated that the polyclonal B cell activation and nonspecific immunosuppression may be uncoupled events induced by different parasite products. The polyclonal lymphocyte activation was induced with variant antigen isolated by either ion exchange or lentil lectin column chromatography and by variant antigen isolated from antigenically dissimilar Trypanosoma brucei rhodesiense and Trypanosoma brucei brucei clones.