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Suppressor cells in Trypanosoma congolense-infected mice
Advances in Experimental Medicine and Biology
|January 1, 1979
Summary
Mice infected with Trypanosoma congolense exhibit potent spleen cell activity that suppresses normal lymphocyte responses. This immunosuppression is primarily mediated by non-T cells, indicating a complex immune evasion strategy.
Area of Science:
- Immunology
- Parasitology
- Cell Biology
Background:
- Trypanosoma congolense infections can lead to immunosuppression.
- Understanding the mechanisms of immunosuppression is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the nature of spleen cells responsible for suppressing lymphocyte stimulation in mice infected with T. congolense.
- To characterize the cell types and properties involved in this immunosuppressive activity.
Main Methods:
- Spleen cells from infected mice were co-cultured with normal spleen cells and mitogens or allogeneic cells.
- Cell dilution studies were performed to assess suppressor activity.
- Spleen cell populations were treated with mitomycin-C, anti-Thy.1 sera and complement, carbonyl iron, or nylon columns to identify suppressor cell characteristics.
Main Results:
- Spleen cells from T. congolense-infected mice strongly suppressed lymphocyte stimulation.
- Suppressor activity was extremely potent, as shown by cell dilution studies.
- Mitomycin-C treatment significantly reduced suppressor activity, suggesting a role for proliferating cells.
- Treatment with anti-Thy.1 sera and complement did not affect suppressor activity.
- Removal of carbonyl iron-binding cells or nylon-adherent cells partially reduced suppressor activity, but did not abolish it.
Conclusions:
- T. congolense infection induces potent immunosuppression mediated by spleen cells.
- The suppressor cells are likely not T cells (Thy.1 positive).
- The suppressor cells may involve proliferating cells (sensitive to mitomycin-C) and potentially include cells with characteristics of both adherent and non-adherent populations.