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

1.LEC大鼠免疫异常的研究。(1)LEC大鼠胸腺T细胞由CD4^+CD8^+ T细胞向CD4^+CD8^- T细胞的成熟过程存在障碍，而向CD4^-CD8^+ T细胞的成熟过程正常。结果，他们胸腺中的CD4^+CD8^- T细胞消失，外周血中的CD4^+CD8^- T细胞显著减少。(2) CD4^+CD8^+和CD4^-CD8^- T细胞中T细胞受体的表达均正常。此外，ⅱ类抗原在胸腺中的表达也是完整的。(3)对T非依赖性抗原的抗体产生正常，而对T依赖性抗原的抗体产生明显抑制，说明辅助性T细胞的功能存在缺陷。然而，杀伤T细胞的功能是保守的。(4)与正常大鼠比较，IL-2、IL-4的表达明显降低。弓形虫感染后腹腔巨噬细胞保护性免疫及热休克蛋白（HSP-65）表达的研究。弓形虫)在LEC大鼠中。(1)与免疫正常的先天性LEA大鼠相比，LEC大鼠对弓形虫感染明显易感。因此，提示CD4^+CD8^- T细胞在大鼠和小鼠体内对弓形虫的保护性免疫中也起重要作用。(2)与LEA大鼠相比，感染弓形虫的LEC大鼠腹腔巨噬细胞中HSP-65的表达明显减弱。由此可见，在小鼠系统中，对弓形虫的保护性免疫潜力与HSP-65的表达程度存在明显的相关性。此外，我们证明CD4^+CD8^- T细胞在大鼠和小鼠中也参与保护性免疫和热休克蛋白65的表达。

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.