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Plasma of cattle infected with Trypanosoma vivax IL2337 was analysed for the presence of bovine tumour necrosis factor (TNF) by EIA in which TNF was captured by a monoclonal antibody (MoAb BC9) and detected by a rabbit polyclonal antiserum. At week 2-3 post infection (p.i.) only a low activity was detected. Therefore, an alternative approach was used in which TNF production was measured ex vivo. Monocytes from T. vivax IL2337-infected cattle manifested a strong TNF production which peaked around week 2 1/2 p.i. Monocytes from pre-infection controls did not produce significant concentrations of TNF. In contrast to the strong production of TNF by monocytes from cattle infected with T. vivax IL2337, TNF production was not detected from monocytes of cattle infected with Trypanosoma congolense ILNat 3.1. Trypanosomiasis due to these parasites differs in the degree if anaemia as indicated by packed cell volume (PCV). T. vivax IL2337 causes a severe, acute PCV fall whereas T. congolense ILNat 3.1. causes a more gradual fall in PCV.

Lymph node cells derived from T. brucei-infected mice fail to produce interleukin 2-(IL2) subsequent to a potent mitogenic trigger and actively suppress the capacity of normal cells to produce IL2 in co-culture experiments. The depletion of Thy-1+ cells does not decrease but rather increases the suppressive potential of the LNC derived from infected mice. A T cell-enriched nylon wool-nonadherent fraction, on the other hand, is not suppressive. The suppression of IL2 production is promptly restored by the addition of prostaglandin synthesis inhibitors suggesting a key role of the prostaglandin-producing macrophages. Our data indicate that such macrophages do not act indirectly through the induction of suppressor T cells, but rather directly interfere with the normal lymph node cells. In contrast to the essential role of prostaglandins in the impairment of IL2 production, these mediators are not involved in the suppression of IL2 receptor expression. Lymph node cells derived from Trypanosoma brucei-infected mice fail to produce interleukin 2 (IL2) subsequent to a potent mitogenic trigger and actively suppress the capacity of normal cells to produce IL2 in co-culture experiments. The depletion of Thy-1+ cells does not decrease but rather increases the suppressive potential of the LNC derived from infected mice. A T cell-enriched nylon wool-nonadherent fraction, on the other hand, is not suppressive. The suppression of IL2 production is promptly restored by the addition of prostaglandin synthesis inhibitors suggesting a key role of the prostaglandin-producing macrophages. Our data indicate that such macrophages do not act indirectly through the induction of suppressor T cells, but rather interfere directly with the normal lymph node cells.