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中国恒河猴反复或长期感染食蟹猴疟原虫后外周血 T 淋巴细胞亚群的特征。

Characterization of peripheral blood T lymphocyte subsets in Chinese rhesus macaques with repeated or long-term infection with Plasmodium cynomolgi.

机构信息

Graduate University of the Chinese Academy of Sciences, Beijing 100049, China.

出版信息

Parasitol Res. 2012 Feb;110(2):961-9. doi: 10.1007/s00436-011-2581-3. Epub 2011 Aug 14.

DOI:10.1007/s00436-011-2581-3
PMID:21842385
Abstract

T lymphocytes play a vital role in antimalaria immunity, but there is little information about the role of T cells in malaria infection. In order to explore the profile of T cells in malaria immunity, we infected Chinese rhesus macaques with the malaria parasite (Plasmodium cynomolgi) and examined the dynamics of T cell subsets. Both repeated and long-term infections were involved. Our results showed that the monkeys in the repeated infection group acquired protective immunity through primary infection, which was evidenced by a much lower parasitemia, milder anemia, and milder fever during reinfection; the monkeys in the long-term infection group also developed protective immunity, but this was not sufficient to eliminate the parasite. The total counts of leukocytes, neutrophils, CD3+ T cells, CD4+ or CD8+ T cells, and naïve and memory CD4+ and CD8+ T cells declined during the acute phase of malaria but increased after the parasite was controlled. The total number of activated CD4+ T cells significantly increased during malaria in animals with a long-term infection, which remained at least 3 months after the termination of malaria. However, the activated CD4+ T cells decreased during the acute phase of infection in the repeated infection group and converted to preinfection levels after malaria was cured. Regulatory CD4+ T cells continued to increase during the malaria infections and quickly reverted to preinfection levels after the parasite was controlled. Our study provides a systematic analysis of the kinetic profiles of T lymphocyte subsets during malaria infections and provides some experimental insight into malaria immunology.

摘要

T 淋巴细胞在抗疟免疫中发挥着至关重要的作用,但关于 T 细胞在疟疾感染中的作用的信息却很少。为了探讨 T 细胞在疟疾免疫中的作用,我们用疟原虫(食蟹猴疟原虫)感染中国恒河猴,并检测 T 细胞亚群的动态变化。这涉及到重复和长期感染。我们的研究结果表明,重复感染组的猴子通过初次感染获得了保护性免疫,这表现在再次感染时寄生虫血症较低、贫血较轻、发热较轻;长期感染组的猴子也产生了保护性免疫,但不足以消除寄生虫。白细胞、中性粒细胞、CD3+T 细胞、CD4+或 CD8+T 细胞、幼稚和记忆 CD4+和 CD8+T 细胞的总数在疟疾的急性期下降,但在寄生虫得到控制后增加。在长期感染的动物中,激活的 CD4+T 细胞的总数在疟疾期间显著增加,至少在疟疾结束后 3 个月仍保持在较高水平。然而,在重复感染组的急性感染期间,激活的 CD4+T 细胞减少,并且在疟疾治愈后恢复到感染前的水平。调节性 CD4+T 细胞在疟疾感染期间持续增加,并在寄生虫得到控制后迅速恢复到感染前的水平。本研究系统分析了 T 淋巴细胞亚群在疟疾感染期间的动力学特征,为疟疾免疫学提供了一些实验见解。

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2
Evaluation of chloroquine therapy for vivax and falciparum malaria in southern Sumatra, western Indonesia.评价印度尼西亚苏门答腊南部地区氯喹治疗间日疟和恶性疟的效果。
Malar J. 2010 Feb 12;9:52. doi: 10.1186/1475-2875-9-52.
3
Investigation of memory responses following Plasmodium chabaudi AS infection in mice distinct in susceptibility to clinical malaria.
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Immunogenetics. 2014 Jan;66(1):15-24. doi: 10.1007/s00251-013-0744-3. Epub 2013 Nov 16.
4
Major histocompatibility complex class I haplotype diversity in Chinese rhesus macaques.中国恒河猴主要组织相容性复合体 I 单倍型多样性。
G3 (Bethesda). 2013 Jul 8;3(7):1195-201. doi: 10.1534/g3.113.006254.
研究不同临床疟疾易感性的伯氏疟原虫 AS 感染小鼠的记忆应答。
Parasitol Res. 2009 Dec;106(1):283-7. doi: 10.1007/s00436-009-1597-4.
4
CD4(+) T cell response in early erythrocytic stage malaria: Plasmodium berghei infection in BALB/c and C57BL/6 mice.早期红细胞期疟疾中的CD4(+) T细胞反应:BALB/c和C57BL/6小鼠的伯氏疟原虫感染
Parasitol Res. 2009 Jul;105(1):281-6. doi: 10.1007/s00436-009-1435-8. Epub 2009 Apr 8.
5
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Parasitol Res. 2009 Feb;104(3):575-82. doi: 10.1007/s00436-008-1232-9. Epub 2008 Oct 31.
6
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7
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8
Regulatory T cells in microbial infection.微生物感染中的调节性T细胞。
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