Basic Research on Protective Immunity against Experimental Hemoprotozoan Infections

本研究利用小鼠模型研究了细胞免疫在巴氏杆菌感染中的作用。在致死性巴氏杆菌感染中，药物治愈的小鼠显示出75%的抵抗B.rodhaini攻击感染的保护，并且体液免疫似乎在免疫的效应期中起主要作用。用抗巴氏杜尔格药治愈首次感染并经攻击感染存活的小鼠对B.radhaini感染显示100%的保护作用，Lyt 1 ^+和Lyt 2 ^+ T细胞可能有助于控制继发感染，而在B.microti感染中，小鼠遭受高寄生虫血症，但从初次感染中自然恢复，nu/nu小鼠和SCID小鼠具有较高的寄生虫血症峰值，未能清除感染。这些结果表明，T淋巴细胞是解决B.microti感染所必需的。用单克隆抗体（mAb）去除CD 4 ^+ T细胞的小鼠有较高的寄生虫血症，不能控制感染，而去除CD 8 ^+ T细胞的小鼠有较高的寄生虫血症， 关于我们 对感染过程没有影响。对照组和去除CD 8 ^+细胞的小鼠的脾细胞培养上清液中IFN-γ的浓度较高，但去除CD 4 ^+细胞的小鼠则没有。用抗IFN-γ mAb治疗感染小鼠显示出比对照组更高的寄生虫血症。这些结果表明，由CD 4 ^+ T细胞产生的IFN-γ至少部分地负责控制B.microti在小鼠中的急性感染。MaB识别B.microti的70，30 kDa抗原并用B.rodhaini攻击，由感染B.microti并用B. rodhaini攻击的小鼠产生。单克隆抗体给药延迟了小鼠寄生虫血症的发作。小鼠经猫等孢子虫卵囊感染后，在第28天对B.microti感染表现出绝对的抵抗力。猫I.felis感染诱导的CD 4 ^+ T细胞对B.microti的免疫保护作用。B.rodhaini感染对肾脏和肝脏的损害较B.microti感染严重。免疫组化显示系膜基质和沿着肾小球基底膜可见电子致密沉积物，这些沉积物被认为是免疫复合物。少

Role of cell-mediated immunity in Babesia infection was investigated using mouse models in the present study. In lethal Babesia rodhaini infection, drug-cured mice showed 75% protection against challenge infection with B.rodhaini and a humoral immunity appears to be major role in the effector phase of immunity. Mice which were cured first infection with anti-Babesia durg and survived with challenge infection, showed 100% protection against B.radhaini infection, Lyt1^+ and Lyt2^+ T cells may contribute in controlling secondary infection.In B.microti infection, while mice sufferd high parasitemia, but recovered naturally from their primary infection, nu/nu mice and SCID had a higher peak parasitemia and failed to clear the infection. These results demonstrated that T lymphocytes are necessary for the resolution of B.microti infection. Mice depleted of CD4^+ T cells with monoclonal antibody (mAb) had high parasitemia and failed to control the infection, while depletion of CD8^+ cells had … More no effect on the course of infection. Culture supernatants of spleen cells from control and CD8^+ cells depleted, but not from CD4^+ depleted mice, showed high concentration of IFN-gamma. Treatment of infected mice with anti-IFN-gamma mAb showed higher parasitemia than that of the control group. These results suggest that IFN-gamma produce by CD4^+ T cells, at least in part, is responsible for the control of acute infection with B.microti in mice.Mab, recognizing 70,30 kDa antigens of B.microti and challenged with B.rodhaini, was produced from mice infected with B.microti and challenged with B.rodhaini. Administration of the mAb gave the delay of onset of parasitemias in mice. Mice which were exposed to oocysts of Isospora felis, showed absolute resistance against B.microti infection on 28th day post-exposure of oocysts. CD4^+ T cells induced by I.felis infection provides mice protection against B.microti.Pathological changes were examined in the kidneys and liver of mice of two babesioses. Severe damages to kidneys and liver were observed in B.rodhaini infection rather than in B.microti infection. Electron-dense deposits were demonstrated in the mesangial matrix and along the glomerular basement membrane and these deposits were suggested as immune complexes by immunohistochemistry. Less