Braunfuchsová P, Salát J, Kopecký J
Institute of Parasitology, Academy of Sciences of the Czech Republic and Faculty of Biological Sciences, University of South Bohemia, Branisovská 31, 370 05, Ceské Budejovice, Czech Republic.
Int J Parasitol. 2001 May 15;31(7):681-6. doi: 10.1016/s0020-7519(01)00134-5.
Microsporidia are obligate intracellular parasites that cause opportunistic infections in immunocompromised patients. The role of two main T cell subsets in anti-microsporidial immunity has been studied using an Encephalitozoon cuniculi-severe combined immunodeficient (SCID) mouse model. Whereas SCID mice reconstituted with CD4+ T lymphocyte-depleted naive BALB/c splenocytes resolved the infection, adoptive transfer of CD8+ T cell-depleted splenocytes failed to protect the animals against a lethal E. cuniculi infection. Splenocytes from E. cuniculi-immune mice specifically killed syngeneic infected macrophages in a short-term 51Cr-release assay. These results suggest the crucial role of cytotoxic T lymphocytes in the protection against E. cuniculi infection.
微孢子虫是专性细胞内寄生虫，可在免疫功能低下的患者中引起机会性感染。使用兔脑炎微孢子虫-重症联合免疫缺陷（SCID）小鼠模型研究了两种主要T细胞亚群在抗微孢子虫免疫中的作用。用CD4+T淋巴细胞耗尽的幼稚BALB/c脾细胞重建的SCID小鼠可清除感染，而CD8+T细胞耗尽的脾细胞的过继转移未能保护动物免受致死性兔脑炎微孢子虫感染。在短期的51Cr释放试验中，来自兔脑炎微孢子虫免疫小鼠的脾细胞特异性杀伤了同基因感染的巨噬细胞。这些结果表明细胞毒性T淋巴细胞在抵抗兔脑炎微孢子虫感染的保护作用中起关键作用。
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