Abstract
Host granulomatous inflammation in murine schistosomiasis mansoni is a T cell-mediated immune response, which, at the chronic stage of the disease, undergoes T suppressor lymphocyte-dependent modulation. This phenomenon was studied in vitro. Spleen cells of mice undergoing modulation (20 wk of infection) when mixed with spleen cells of animals exhibiting vigorous granulomatous responses (8 wk of infection) abrogated in vitro migration inhibition factor (MIF) production by the latter. Characterization of the delayed-type hypersensitivity T lymphocytes involved in lymphokine production showed that they belonged to the Lyt-1+ subset and did not express I region-encoded antigens. T lymphocytes involved in the suppression of MIF activity belonged to the Lyt-2+ subpopulation of cells which expressed I-J- and I-C-subregion determinants. The modulation of the granulomatous hypersensitivity response in mice is probably the result of T-T cell interaction with subsequent regulation of inflammatory lymphokine production.