Mechanisms of opportunistic infection with protozoa in CD4^+T cell deficient rats

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1.Research for the immunological abnormality in LEC rats. (1)LEC rats had a disturbance of T cell maturation from CD4^+CD8^+ T cells to CD4^+CD8^- T cells in their thymuses,while maturation to CD4^-CD8^+ T cells was normal. As the result,CD4^+CD8^- T cells disappeared in their thymuses and remarkably reduced in their peripheral blood. (2)The expression of T cell receptors were normal in both CD4^+CD8^+ and CD4^-CD8^- T cells.Further, the expression of class-II antigen in their thymuses was also intact. (3)Antibody production to T-independent antigens was normal,whereas that to T-dependent antigens was clearly suppressed,indicating that the function of helper T cells was defective.However,the function of killer T cells was conserved. (4)Productions of IL-2 and IL-4 were markedly depressed,compared with normal rats.2.Research for protective immunity and expression of heat-shock protein(HSP-65)on peritoneal macrophages after infection with Toxoplasma gondii(T.gondii)in LEC rats. (1)LEC rats were clearly susceptible to infection with T.gondii compared with immunocompetent congenic LEA rats. Thus,it was suggested that CD4^+CD8^- T cells play an important role for protective immunity against T.gondii also in rat as well as in mice. (2)The expression of HSP-65 on peritoneal macrophages of LEC rat infected with T.gondii was extremely attenuated compared with that of LEA rats.From these bases,obvious correlation existed between the potential of protective immunity against T.gondii and the degree of expression of HSP-65 as was seen in murine systems.Moreover,we demonstrated that CD4^+CD8^- T cells perticipated in both protective immunity and the expression of HSP-65 also in rats as well as in mice.