Activated macrophages (Mφ) appear responsible for at least part of the concomitant resistance in mice infected with Schistosoma mansoni. We found that as murine S. mansoni progressed from acute (8 to 12 wk of infection) to chronic (16 to 214 wk) stages, acquired resistance decreased (57% resistance to challenge with cercariae at 8 wk vs 28% by 24 wk, p <0.05), as did macrophage activation (21% ± 2 killing of schistosomula by 8 wk Mφ vs 8% ± 2 for 24 wk Mφ, p <0.01). T cells from the spleens of 8 wk-infected mice were capable of activating Mφ from naive animals when stimulated with worm antigens (24% ± 2 kiling vs 8% ± 2 induced by normal T cells, p <0.01); T cells obtained from 24 wk-infected mice did not activate Mφ (13% ± 2 killing). Furthermore, T cells from 24 wk-infected animals suppressed activation of Mφ by 8 wk T cells. The addition of 105 24 wk T cells to 3 x 105 antigen-stimulated 8 wk T cells reduced subsequent Mφ killing from 27% ± 4 to 13% ± 2 (p <0.05). Week 24 T cells (3 x 105) reduced this additionally to 9% ± 1(p <0.01), a value no greater than that of unstimulated Mφ. The subpopulation of T cells responsible for suppression of Mφ activation was Lyt-2+1- nonadherent T cells. Cyclophosphamide treatment of chronically infected mice resulted in enhanced resistance (41%), Mφ activation (18% ± 1 killing), and T cell activation of naive Mφ (10% ± 1 killing). Thus, during chronic S. mansoni infection, resistance to reinfection wanes in parallel to and perhaps because of development of suppressor T cells that interfere with T-dependent Mφ activation.
|Original language||English (US)|
|Number of pages||5|
|Journal||Journal of Immunology|
|Publication status||Published - 1984|
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