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机构地区:[1]中国预防医学科学院寄生虫病研究所
出 处:《中国寄生虫学与寄生虫病杂志》1991年第1期50-54,共5页Chinese Journal of Parasitology and Parasitic Diseases
摘 要:用非致死性约氏疟原虫对C57BL/6J、NIH和ICR小鼠进行初次感染和对初次感染阴转后的NIH小鼠再次感染,观察其原虫血症并测定小鼠感染过程中其脾脏淋巴细胞在Con A或约氏疟原虫抗原诱生的白细胞介素-2(IL-2)水平。结果:(1)C57BL/6J、NIH和ICR小鼠感染前Con A诱生的IL-2水平(SI的X±SE)分别为223.71±19.32、122.13±28.91和72.76±30.60,初次感染后最高原虫血症(%的X±SE)分别为2.70±0.29、14.50±2.75和31.30±1.80;提示,这3种小鼠感染前固有的Con A诱生的IL-2水平高低可能影响其对约氏疟原虫初次感染的易感性。(2)NIH小鼠初次接种约氏疟原虫后34d,抗原诱生的IL-2才出现;而再次接种后d_3、d_(19)IL-2水平升高,并使这些小鼠对再次感染有明显的抵抗力。这提示抗原诱生的IL-2与鼠疟保护性免疫的调节有关。C57BL/6J, NIH and ICR mice were inoculated with nonlethal P. yoelii (BY 265 strain) and NIH mice which had recovered from primary infection were reinocizlated with the same parasite. The parasitemia of the mice was observed and IL-2 production by spleen lymphocytes of the mice upon Con A or P. yoelii antigen stimulation was detected at different intervals throughout primary infection and reinfection. The IL-2 level was measured by the microassay bzsed on incorporation of H-TdR into CTLL2. The main results were as follows: (1) There were marked differences in both the Con A-induced IL-2 production and the parasitemia between C57BL/6J, NIH and ICR mice. The Con A-induced IL-2 levels (X± SE of SI) in C57BL/6J, NIH and ICR mice before primary infection were 223.7±19.32, 122.12±28.91 and 7226±30.60 respectively. The maximum parasitemia (X± SE of %) in C57BL/6J, NIH and ICR mice after primary infection were 2.7%±0.29%, 14.50% ±2.75% and 31.30%±1.80% separately. It suggests that the innate Con A-induced IL-2 levels in the three strains of mice might be one of the factors influencing their susceptibility to P. yoelii primary infection. (2) There was significant depression in the capacity of releasing IL-2 upon Con A stimulation 3, 10 and 15 days after NIH mice had been inoculated with P. yoelii; after that, it was followed by the gradual resumption of the Con A-induced IL-2 production. P. yoelii antigen-induced IL-2 was only detected by d34 after inoculation. In contrast, when NIH mice which had been recovered from primary infection were reinoculated with the same parasite, the animals were partly re3istant to reinfection and there was no decrease in Con A-induced IL-2 production after reinocu-lation and the enhancement of IL-2 production upon specific antigen stimulation 3 and 19 days after reinoculation. The findings suggest that the parasitespecific splenic lymphocytes capable of releasing IL-2 upon antigen stimulation appear in the late st?.ge of primary infection and the lymphocytes possessing memory functio
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