GAMMA INTERFERON-DEPENDENT TEMPORARY RESISTANCE TO ACUTE TOXOPLASMA-GONDII INFECTION INDEPENDENT OF CD4(+) OR CD8(+) LYMPHOCYTES

It is well established that resistance to acute primary Toxoplasma gondii infection is mediated by a gamma interferon (IFN-gamma)-dependent mechanism. The present in vivo experiments were undertaken to investigate the cellular basis for this resistance. We show here that immunocompetent T. gondii-infected C57BL/6 (B6) mice treated with anti-IFN-gamma or with anti-Thy-1 or anti-asialo-GM1 antibodies die sooner than infected mice treated with antibodies that deplete both CD4(+) and CD8(+) T lymphocytes. Thy-1(+) CD4(-) CD8(-) cells accumulated in the peritoneal cavities of B6 mice during the early stages of an intraperitoneal infection but did not accumulate in sham-infected control mice, and substantial numbers of Thy-1(+) CD4(-) CD8(-) cells were recovered from the peritoneal cavities of infected B6 mice treated with antibodies that depleted CD4(+) and CD8(+) lymphocytes. Depletion of Thy-1(+) cells reduced IFN-gamma to undetectable levels, whereas depletion of CD4+ and CD8(+) cells did not reduce IFN-gamma levels. Thus T. gondii infection in immunocompetent B6 mice elicits Thy-1(+) CD4(-) CD8(-) cells which either produce protective IFN-gamma themselves or control its production by other cells. It is likely that the function of these Thy-1(+) CD4(-) CD8(-) cells is to control T. gondii tachyzoites during the early stages of primary infection before specific CD4(+) - and/or CD8(+)-dependent immunity develops.