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From the WHO Immunology Research and Training Center, Lausanne Section, the Department of Biochemistry, University of Lausanne, Epalinges and Geneva Section, Centre de Transfusion, Hôpital Cantonal, Geneva, Switzerland
Abstract
In vivo induction of autoantibodies by polyclonal B cell activators has been suggested to be the direct consequence of the polyclonal B lymphocyte activation. Since the appearance of various autoantibodies represents a common feature of some parasitic infections, the possibility that such autoantibodies develop as a result of the stimulation of polyclonal antibody synthesis was tested in mice infected experimentally with Trypanosoma brucei brucei (T. brucei).
Polyclonal antibody production in the spleen was measured by the Cunningham plaque-forming cell (PFC) assay with SRBC, TNP-SRBC, and FITC-SRBC as indicator cells. Compared with normal mice, T. brucei-infected animals displayed a marked increase in the number of PFC to TNP, FITC, or SRBC. The level of polyclonal antibody synthesis was correlated to the number of T. brucei injected and to the number of parasites in circulating blood. The observed B lymphocyte activation is not dependent upon the influence of T cells since infection of athymic nu/nu mice also led to polyclonal antibody synthesis. Stimulation of polyclonal antibody synthesis was also observed after T. brucei infection of C3H/HeJ mice, a strain of mice that is nonresponsive to bacterial lipopolysaccharides. Therefore, it is unlikely that the lipopolysaccharides component of endogenous Gram-negative bacteria play an important role in the observed proliferation and differentiation of B lymphocytes.
Autoimmune responses to DNA, red blood cells, and thymocyte antigens were observed in mice infected with T. brucei and the kinetics of their formation was parallel to the development of the polyclonal B cell activation.
Footnotes
1 This work has been supported by the Swiss National Research Foundation (Grant No. 32600.74), The Dubois Ferrière Dinu Lipatti Foundation, and the World Health Organization.
2 Supported in part by the Atomic Energy Bureau, Science and Technology Agency, Tokyo, Japan.
3 Address correspondence to: Jacques Louis, WHO Immunology Research and Training Centre, Department of Biochemistry, University of Lausanne, chemin des Boveresses, 1066 Epalinges, Switzerland.
4 Supported by a World Health Organization Research Training Grant.
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