Expression of 65 000 MW Heat-shock Protein in SCID Mice Infected with Toxoplasma gondii after Transplantation of Mouse Fetal Thymus

Abstract

Heat-shock proteins (HSPs) are evolutionarily highly conserved polypeptides. They are immunodominant antigens in a wide variety of bacteria and parasites. We reported that the induction of 65 000 MW HSP (HSP65) plays an important role in developing protective immunity against infection with Toxoplasma gondii. Here, we examined the role of T cells in the expression of HSP65 and in the acquisition of protective immunity in SCID mice transplanted with fetal thymus or liver cells from syngeneic C.B-17 mice and infected with T. gondii. When SCID mice lacking mature T and B cells were transplanted with fetal liver cells (FLT-SCID mice), T and B lymphopoiesis were reconstituted to the level of normal mice, whereas only T lymphopoiesis was reconstituted in SCID mice grafted with a fetal thymus (TG-SCID mice). These mice were infected with the Beverley strain bradyzoites of T. gondii 7 days after immunization with Toxoplasma homogenate. Immunization effect did not occur in untreated SCID mice (UT-SCID mice), all of which died within 2 weeks after infection. HSP65 was not expressed in their macrophages. The survival of TG-SCID mice was significantly prolonged by immunization as compared with that of the immunized UT-SCID mice, and all the immunized FLT-SCID mice acquired complete resistance as well as the immunized C.B-17 mice. HSP65 was expressed in macrophages of TG-SCID mice after immunization, and much higher in those of FLT-SCID mice. These results indicate that T cells play a crucial role in the expression of HSP65 and in the induction of protective immunity against infection with T. gondii.