GAMMA-DELTA T-CELLS FUNCTION IN CELL-MEDIATED-IMMUNITY TO ACUTE BLOOD-STAGE PLASMODIUM-CHABAUDI ADAMI MALARIA

To determine whether gamma delta T cells are essential for the resolut ion of acute Plasmodium chabaudi adami (P.c. adami) malaria, we deplet ed gamma delta T cells from C57BL/6 mice with hamster monoclonal anti- TCR gamma delta Ab treatment. During the period in which control mice that had received normal hamster IgG completely resolved infections, g amma delta T cell-depleted mice were unable to suppress their infectio ns. Because the number oi splenic CD4(+) alpha beta T cells in these a nti-TCR-gamma delta-treated mice with nonresolving malaria was similar to control mice, it appears that CD4(+) alpha beta T cells alone cann ot mediate early resolution even though they are known to play a criti cal role in immunity to blood-stage malaria. Mice treated with anti-CD 4 mAb also failed to resolve P.c. adami malaria. Depletion of CD4(+) a lpha beta T cells from the spleens of infected mice resulted in minima l expansion of the splenic CD4(-) gamma delta T cell subset compared w ith infected control mice. Together, these findings indicate that acti vation of the gamma delta T cell subset, which requires the presence o f CD4(+) alpha beta T cells, is essential for resolution of acute P.c. adami malaria. To determine whether gamma delta T cells require eithe r Abs or B cells to achieve their protective activity, B cell-deficien t J(H)D mice were treated with the same depleting anti-TCR-gamma delta Abs. Whereas control J(H)D mice injected with hamster IgG resolved ac ute P.c. adami malaria, J(H)D mice depleted of gamma delta T cells fai led to do so. We conclude that gamma delta T cells suppress P.c. adami parasitemia by mechanisms of immunity independent of Ab and B cells.