摘要
为研究ＩＬ—２在克氏锥虫感染过程中出现的免疫抑制机制中的作用，８只克氏锥虫感染的Ｃ３Ｈ／ＨｅＪｎ小鼠每日皮下注射两次，每日总量５０００μ重组人ｒＩＬ－２；对照组相同数量小鼠皮下注射等量的无钙、镁离子的ＰＢＳ。实验结果表明ｒＩＬ－２注射组小鼠脾细胞对羊红细胞的反应能力由ＰＢＳ注射鼠的１５。２％提高到９３。５％（Ｐ＜０．０５）。相当接近于正常的未感染小鼠的空斑形成细胞数。ｒＩＬ－２注射组小鼠仅表现轻度降低的寄生虫血症，其动态变化在两组间未显示出差异。除ＰＢＳ组的１只小鼠在感染后第３６ｄ死亡外，ｒＩＬ－２以及ＰＢＳ注射组的其它动物都在克氏锥虫急性感染期存活。尽管ｒＩＬ－２注射并未明显地提高克氏锥虫急性感染期Ｃ３Ｈ／ＨｅＪｎ小鼠的抗虫保护性免疫，本实验提示ＩＬ－２不足是克氏锥虫急性感染期Ｃ３Ｈ／ＨｅＪｎ小鼠非特异性免疫抑制的原因之一。
In order to provide in vivo evidences whether IL-2 deficie dncy is involved in the mechanism of immunosuppression occurred during acute Trypanosoma cruzi infection, in vivo effect of hrlL-2 was examined by comparing the anti-SRBC and anti-T. cruzi responses indicated by parasitemia and longevity between two groups of T. cruzi infected mice which were given rIL-2 or PBS respectively. Nineteen female C3H/HeJn mice,38 days of age were used in the extperiment. Sixteen infected mice received 1,000 bloodform trypomastigotes of(BFT) the Brazil strain of T. cruzi by the tail intravenous route.For the experimental group, 8 infected mice were given 5000 U hrIL-2 cubcutaneously two times a day from the 7th day to the 35th day after infection. For the control group, 8 infected mice received equal volume of Ca++, Mg++ free PBS only. Three mice were as uninfected normal control. After in vivo IL-2 administration, the response of spleen cells of T. cruzi infected mice to SRBC was greatly stimulated. The responding ability to SRBC increased from 15.2% in PBS group to 93.5% in IL-2 group (P<0.05), very near the level of direct plaque-forming cells(DPFC) in the normal uninfected mice. Only slightly lower group level of parasitemia can be found in IL-2 receiving group, however, the difference was not statistically significant(P>0.05). In addition, the peak and decrease of the BFT did not show any timing differences between IL-2 and PBS group. Except one mouse in PBS group died on the 36th day after infection, all other animals survived during the acute phase of T. cruzi infection. Though hrIL-2 failed to improve parasitemia and longevity effectively, it demonstrated in vivo that deficient production of IL-2 in T.cruzi infection was indeed at least partially responsible for the nonspecific immunosuppression. The possible explanation for the unaffected protective immunitv after rlL-2 administration were discussed.
出处
《寄生虫与医学昆虫学报》
CAS
1994年第4期1-6,共6页
Acta Parasitologica et Medica Entomologica Sinica
