Goyal M, Ganguly N K, Mahajan R C
Department of Parasitology, Postgraduate Institute of Medical Education and Research, Chandi Garh, India.
Med Microbiol Immunol. 1989;178(5):269-78. doi: 10.1007/BF00191061.
Both humoral and cell-mediated immune responses were studied in reactivated toxoplasma infection in mice. The infection was established by immunosuppressing chronically infected animals by thymectomy followed by irradiation. The reactivated infection was confirmed by reappearance of toxoplasma tachyzoites in peritoneal exudate. The animals survived until the 8th day post thymectomy. The percentage of splenic T lymphocytes was depressed after 4th day post thymectomy in both the uninfected thymectomized and infected immunosuppressed animals as compared to the intact uninfected controls and intact chronically infected animals. However, there was no significant change (P greater than 0.05) between the uninfected immunosuppressed control and infected immunosuppressed mice. When the infection progressed to more acute phase there was significant depression (P less than 0.01) in the percentage of T lymphocytes in comparison to the uninfected thymectomized mice. However, there was no change in the percentage of B lymphocytes (P greater than 0.05). The function of lymphocytes as assessed by blast transformation was depressed in the presence of nonspecific mitogens, i.e. phytohemagglutinin and concanavalin A until the end of the study. The response to toxoplasma antigen was increased during early stages in the infected immunosuppressed mice (stimulation index = 4.15 +/- 0.1 and 4.5 +/- 0.15 on 4th and 6th day post thymectomy). On the 8th day post thymectomy, there was a sudden fall in the stimulation index (3.5 +/- 0.11). The antitoxoplasma antibodies as detected by indirect hemagglutinin and fluorescence analysis and enzyme-linked immunosorbent assay (ELISA) tests and toxoplasma-specific IgM antibodies as detected by ELISA test were present throughout the study period though at low levels. The significance of these findings is discussed.
在小鼠弓形虫再激活感染中研究了体液免疫和细胞介导的免疫反应。通过对慢性感染动物进行胸腺切除后照射来建立免疫抑制,从而引发感染。通过腹膜渗出液中再次出现弓形虫速殖子来确认再激活感染。这些动物存活至胸腺切除术后第8天。与完整未感染对照和完整慢性感染动物相比,未感染胸腺切除和感染免疫抑制动物在胸腺切除术后第4天脾脏T淋巴细胞百分比均降低。然而,未感染免疫抑制对照和感染免疫抑制小鼠之间无显著变化(P大于0.05)。当感染进展到更急性期时,与未感染胸腺切除小鼠相比,T淋巴细胞百分比显著降低(P小于0.01)。然而,B淋巴细胞百分比无变化(P大于0.05)。在整个研究期间,通过有丝分裂原转化评估的淋巴细胞功能在存在非特异性有丝分裂原即植物血凝素和刀豆球蛋白A的情况下受到抑制。在感染免疫抑制小鼠的早期阶段对弓形虫抗原的反应增加(胸腺切除术后第4天和第6天刺激指数分别为4.15±0.1和4.5±0.15)。胸腺切除术后第8天,刺激指数突然下降(3.5±0.11)。通过间接血凝、荧光分析和酶联免疫吸附测定(ELISA)检测到的抗弓形虫抗体以及通过ELISA检测到的弓形虫特异性IgM抗体在整个研究期间均存在,尽管水平较低。讨论了这些发现的意义。