Immunopotentiatroy Effects of TLA and Obioactin on the Acquired Immunodeficiency Syndroms (AIDS) in animals

据报道，弓形虫能激发对啮齿动物疟疾和巴贝斯虫病的非特异性抵抗力。接受弓形虫裂解抗原(TLA)系统治疗的小鼠对伯氏疟原虫和罗德海尼巴贝斯虫的感染具有高度的抵抗力。因此，对TLA致敏动物的淋巴细胞、自然杀伤(NK)细胞和淋巴因子激活的杀伤(LAK)细胞的行为的研究可能有助于阐明抵抗原虫和肿瘤感染的因素。成年BALB/C小鼠每隔2周肌肉注射两次TLA致敏后，脾、肝和外周血中Sig(+)、Thy-1(+)、Lyt-2、2(+)和asialo GM1(+)细胞的数量比未致敏的小鼠增加2~4倍。当Tla致敏和非致敏的小鼠接种巴贝斯虫时，Tla致敏的小鼠中有4只(40%)存活下来，而未致敏的对照组小鼠没有一只存活…感染后14天以上。相比之下，TLA对裸鼠的致敏作用对小鼠的存活没有影响，小鼠的存活不超过12天。在TLA致敏和非致敏的Bala/c小鼠中，胸腺Thy-1，2(+)细胞在感染后10天内减少了近80%。同时，致敏小鼠和非致敏小鼠的脾、肝和外周血中B细胞、T细胞和NK细胞的数量均增加。特别值得注意的是，TLA致敏和非致敏小鼠的脾和血中Lyt-2、2细胞数量增加，脾、肝和血中NK细胞数量增加。将TLA致敏和未致敏小鼠的脾细胞在有或无TLA的条件下培养6天，用NK不敏感的P-815靶细胞和NK敏感的YAC-1靶细胞进行细胞毒试验，结果表明TLA致敏的小鼠脾细胞具有较高的细胞毒作用。结果表明，在TLA致敏的脾细胞培养中加入TLA可刺激杀伤细胞的产生，如淋巴因子激活的杀伤细胞(LAK)和NK样LAK和/或NK细胞。因此，TLA致敏小鼠对原虫感染的抵抗力不仅可能与Thy-1、2(+)和asialo GM1(+)细胞数量的增加有关，还可能与这些细胞类型的数量和质量变化有关。较少

Toxoplasma gondii has been reported to stimulate non-specific resistance to rodent malaria and babesia diseases. Mice that were treated systemically with Toxoplasma lysate antigen (TLA) were highly resistant to infection with Plasmodium berghei and Babesia rodhaini. Consequently, studies of the behavior of lymphocytes and natural killer (NK) cells and lymphokines activated killer (LAK) cells from TLA sensitized animals may clarify the factors responsible for resistance to infection with protozoan parasites and with tumors.When adult BALB/C mice were sensitized with two intramuscular injection of TLA at 2 week interval, the numbers of Sig(+), Thy-1(+), Lyt-2, 2(+), and asialo GM1(+) cells in the spleen, liver and peripheral blood increased by 2 to 4 times over those found in unsensitized mice of the same age. When TLA-sensitized and unsensitized mice were inoculated with Babesia, 4 of 10(40%) of the TLA-sensitized mice survived infection, while none of the unsensitized control mice live … More d longer than 14 days after infection. By contrast sensitization of nude mice with TLA has no effect on survival, and mice did not live more than 12 days. The number of thymic Thy-1, 2(+) cells decreased in TLA-sensitized and unsensitized BALA/c mice by almost 80% within 10 days after infection. During the same time, the numbers of B cells, T cells, and NK cells increased in the spleen, liver and peripheral blood of both sensitized and unsensitized mice. Especially notable were increases in the numbers of Lyt-2,2 cells in the spleen and blood and increases in numbers of NK cells in the spleen, liver and blood in both TLA-sensitized and unsensitized mice. When spleen cells from TLA-sensitized and unsensitized mice were cultured in the presence or absence of TLA for 6 days, assays for cytotoxicity using NK-insensitive P-815 target cells and NK-sensitive YAC-1 target cells demonstrated higher rates of cytotoxicity in cultures of TLA-sensitized spleen cells. The present results showed clearly that addition of TLA to cultures of TLA-sensitized spleen cells stimulates production of killer cells, such as lymphokine activated killer (LAK) cells and NK-like LAK and/or NK cells. Consequently, resistance of TLA sensitized mice to protozoan infection may be mediated not only by increases in the numbers of Thy-1, 2(+) and asialo GM1(+) cells, but also by quantitative and qualitative variations in these cell types. Less