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Exacerbation of Plasmodium chabaudi malaria in mice by depletion of TCR alpha beta+ T cells but not TCR gamma delta+ T cells.

机译:通过消耗TCRαβ+ T细胞(而不是TCRγδ+ T细胞)来破坏小鼠的chabaudi疟原虫疟疾。

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摘要

Although gamma delta T cells are found in increased numbers in the spleens of humans and mice infected with malaria, it is not known if these cells are necessary components of an effective immune response. The surface phenotype of spleen cells obtained from mice infected with avirulent Plasmodium chabaudi adami or virulent Plasmodium chabaudi chabaudi were examined using anti-delta or anti-alpha beta T-cell-specific reagents and flow cytometry. Levels of parasitaemia, red blood cell (RBC) counts, and survival times were followed in mice depleted of tumour necrosis factor (TCR)gamma delta+ or TCR alpha beta+ T cells. Numbers of gamma delta T cells increased in the spleens of control antibody-treated infected mice, but not in mice depleted of TCR gamma delta+ or TCR alpha beta+ T cells. Mice depleted of gamma delta T cells had levels of parasitaemia, RBCs, and survival rates similar to control antibody-treated mice. However, mice depleted of TCR alpha beta+ T cells had higher levels of parasitaemia, lower RBC counts, and decreased survival rates. These results indicate that TCR alpha beta+ but not TCR gamma delta+ T cells play an essential role in host defense against P. chabaudi infection in mice.
机译:尽管在感染疟疾的人和小鼠的脾脏中发现了γ-δT细胞数量增加,但尚不清楚这些细胞是否是有效免疫应答的必要组成部分。使用抗δ或抗αβT细胞特异性试剂和流式细胞仪检查从感染无毒疟原虫阿巴米或强毒疟原虫的小鼠中获得的脾细胞表面表型。在消耗了肿瘤坏死因子(TCR)γδ+或TCRαβ+ T细胞的小鼠中,追踪寄生虫血症,红细胞(RBC)计数和存活时间。在对照抗体治疗的感染小鼠的脾脏中,γ-δT细胞的数量增加,但在没有TCRγ-δ+或TCRα-β+ T细胞的小鼠中,γδT细胞的数量没有增加。耗竭了γ-δT细胞的小鼠的寄生虫血症,RBC和存活率与对照抗体治疗的小鼠相似。但是,消耗了TCRαβ+ T细胞的小鼠的寄生虫血症水平更高,RBC计数更低,存活率降低。这些结果表明,TCR alpha beta +而不是TCR gamma delta + T细胞在抵抗小鼠霍乱沙门氏菌感染的宿主防御中起重要作用。

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