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通过耗竭TCRαβ⁺ T细胞而非TCRγδ⁺ T细胞加重小鼠查巴迪疟原虫疟疾感染。

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

作者信息

Sayles P C, Rakhmilevich L

机构信息

Trudeau Institute Inc., Saranac Lake, NY 12983, USA.

出版信息

Immunology. 1996 Jan;87(1):29-33.

Abstract

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.

摘要

尽管在感染疟疾的人类和小鼠脾脏中发现γδ T细胞数量增加,但尚不清楚这些细胞是否是有效免疫反应的必要组成部分。使用抗δ或抗αβ T细胞特异性试剂和流式细胞术检测了感染无毒夏氏疟原虫或有毒查氏疟原虫的小鼠脾脏细胞的表面表型。在耗尽肿瘤坏死因子(TCR)γδ+或TCRαβ+ T细胞的小鼠中跟踪疟原虫血症水平、红细胞(RBC)计数和存活时间。在对照抗体处理的感染小鼠脾脏中,γδ T细胞数量增加,但在耗尽TCRγδ+或TCRαβ+ T细胞的小鼠中未增加。耗尽γδ T细胞的小鼠的疟原虫血症水平、红细胞数量和存活率与对照抗体处理的小鼠相似。然而,耗尽TCRαβ+ T细胞的小鼠疟原虫血症水平更高,红细胞计数更低,存活率降低。这些结果表明,TCRαβ+而非TCRγδ+ T细胞在小鼠抵抗查氏疟原虫感染的宿主防御中起重要作用。

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