GAMMA-DELTA T-CELLS PLAY AN IMPORTANT ROLE IN HSP65 EXPRESSION AND INACQUIRING PROTECTIVE IMMUNE-RESPONSES AGAINST INFECTION WITH TOXOPLASMA-GONDII

Previously, we reported that the expression of hsp65 within and on hos t macrophages correlates closely with protection against infection wit h Toxoplasma gondii in mice, Herein, we propose that gamma delta T sel ls play a crucial role in the induction of hsp65 and also in the prote ctive immune response to T. gondii. Intraperitoneal inoculation with t his protozoan resulted in hsp65 being expressed on and in host periton eal macrophages and resulted in an increase of T cells bearing the gam ma delta receptor with Thy-1(+) and Thy-1(-) phenotypes in the periton eal cavity and spleen. When mice were depleted of gamma delta T cells by the administration of a mAb, hsp65 expression was markedly decrease d. In contrast, the expression of this protein was rather enhanced and gamma delta T cells were prominently expanded in mice depleted of alp ha beta T cells, The protection in mice treated with the mAb parallele d the magnitude of hsp65 expression. Mice depleted of gamma delta T ce lls died most frequently in the early stages of infection, whereas mos t of those depleted of alpha beta T cells survived the early stages of lethal infection with T,gondii. However, the latter group of mice did not definitely control the T. gondii infection in its late stages. IF N-gamma was not essential for either the expression of hsp65 or the re sistance induced by gamma delta T cells, as demonstrated in mice treat ed with mAb to murine IFN-gamma. These findings indicated that gamma d elta T cells having both the Thy-1(+) and Thy-1(-) phenotypes contribu te to hsp65 expression within and on macrophages in an IFN-gamma-indep endent manner. This, in turn, plays a role in the development oi prote ctive immunity during the early stage of this parasitic infection.