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首页> 外文期刊>Infection and immunity >Polyclonal expansion of peripheral gamma delta T cells in human Plasmodium falciparum malaria.
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Polyclonal expansion of peripheral gamma delta T cells in human Plasmodium falciparum malaria.

机译：人恶性疟原虫疟疾中外周γδT细胞的多克隆扩增。

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Plasmodium falciparum malaria in humans is associated with an increase in the percentage and absolute number of gamma delta T cells in the peripheral blood. This increase begins during the acute infection phase and persists for at least 4 weeks during convalescence. In the present study, 25 to 30% of the gamma delta T cells expressed HLA-DR antigens in vivo and in some patients they proliferated in response to further stimulation by purified human interleukin 2 in vitro. However, there was no in vitro proliferative response to various malarial antigens, including a 75-kDa heat shock protein and a 72-kDa glucose-regulated protein of P. falciparum during the acute infection phase. Cytofluorographic studies showed that although an increase of V delta 1- gamma delta T cells was largely responsible for the expansion of the total number of gamma delta T cells, there was also a proportional increase in V delta 1+ cells. These results were confirmed with anchored PCR and by DNA sequencing to characterize at the molecular level the set of T-cell receptor (TCR) delta mRNAs expressed in the peripheral blood of two patients with high levels of gamma delta T cells. In each case, most of the TCR delta mRNA transcripts corresponded to nonproductively rearranged delta genes (unrearranged J delta or near J delta spliced to C delta). In those sequences which did represent productively rearranged genes, most of the transcripts originated from a V delta 2/J delta 1 joining, as in normal individuals. A minority of transcripts originated from a V delta 1/J delta 1 rearrangement, and one originated from a V alpha 4/J delta 1 rearrangement. Polyclonal activation of gamma delta T cells was inferred from the extensive junctional diversity seen in the delta mRNAs analyzed. Expansion of a heterogeneous set of both V delta 1(-)- and V delta 1(+)-bearing T cells suggests that the elevated levels of gamma delta T cells seen during acute P. falciparum malaria arose from immune responses to multiple distinct parasite antigens or unidentified host factors.
机译：人类的恶性疟原虫疟疾与外周血中γδT细胞的百分比和绝对数量的增加有关。这种增加在急性感染阶段开始，并且在恢复期持续至少4周。在本研究中，有25％到30％的γ-δT细胞在体内表达HLA-DR抗原，并且在某些患者中，它们在体外对纯化的人白介素2的进一步刺激反应而增殖。但是，在急性感染阶段，对各种疟疾抗原，包括恶性疟原虫的75 kDa热休克蛋白和葡萄糖调节72 kDa葡萄糖调节蛋白，没有体外增殖反应。细胞荧光检查研究表明，尽管V delta1-γdelta T细胞的增加是造成γdelta T细胞总数增加的主要原因，但V delta 1+细胞也呈比例增加。这些结果通过锚定PCR和DNA测序证实，以分子水平表征了两名患有高水平γδT细胞的患者外周血中表达的T细胞受体（TCR）δmRNA的表达。在每种情况下，大多数TCR delta mRNA转录物对应于非生产性重排的delta基因（未重排的J delta或接近J delta的C delta剪接）。在那些确实代表生产性重排基因的序列中，大多数转录本都像正常个体一样，源自V delta 2 / J delta 1连接。少数转录本源自V delta 1 / J delta 1重排，而一个转录本源自V alpha 4 / J delta 1重排。 γ-δT细胞的多克隆激活是从在分析的delta mRNA中看到的广泛的连接多样性推断出来的。携带V delta 1（-）和V delta 1（+）的T细胞异质性集合的扩展表明，在急性恶性疟原虫疟疾期间见到的γdelta T细胞水平升高是由于对多种不同寄生虫的免疫反应引起的抗原或未知的宿主因素。

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