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Non‐specific immune responses in CBA/N mice infected with Trypanosoma brucei

CBA/N mice carry a genetic defect which causes a maturational arrest of normal B lymphocyte development, and results in an inability to mount IgM antibody responses against certain T lymphocyte‐independent antigens. These mice were found to survive an experimental infection with Trypanosoma brucei two to three times longer than conventional mice. This enhanced survival does not appear to be related to the level of infection of the host since parasitaemias were similar in all strains tested. In addition, the level of non‐specific polyclonal B cell activation as assessed by the enumeration of anti‐TNP antibody‐producing cells in the spleens of infected animals was found to be similar in CBA/N, CB A/CaT6 and A/J mice. In contrast, the level of circulating immune complex‐like material was lower in CBA/N mice at a time when mice of other strains were dying from the effects of the infection. Finally, although CBA/N mice survive a T. brucei infection for a longer time interval, they exhibit a non‐specific immunosuppression similar to that seen in conventional mice.