EVIDENCE OF ENDOTHELIAL INFLAMMATION, T-CELL ACTIVATION, AND T-CELL REALLOCATION IN UNCOMPLICATED PLASMODIUM-FALCIPARUM MALARIA
EVIDENCE OF ENDOTHELIAL INFLAMMATION, T-CELL ACTIVATION, AND T-CELL REALLOCATION IN UNCOMPLICATED PLASMODIUM-FALCIPARUM MALARIA
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DOI：
10.4269/ajtmh.1994.51.372
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发表时间：
1994-09-01
影响因子：
3.3
通讯作者：
THEANDER, TG
中科院分区：
文献类型：
--
作者：
ELHASSAN, IM;HVIID, L;THEANDER, TG
为了解释急性恶性疟原虫疟疾与外周血细胞在体外对抗原刺激反应的暂时性无能有关的观察结果，我们假设疾病诱导的外周淋巴细胞的重新分配，可能是通过粘附到发炎的内皮细胞。我们测量了32例急性无并发症恶性疟原虫疟疾患者的可溶性内皮炎症标记物和T细胞活化的血浆水平。以及10个健康的、寄生虫血症的对照供体。所有捐助者都是苏丹东部州疟疾流行地区的居民。此外，我们测量了T细胞表面白细胞介素-2受体（CD 25）和淋巴细胞功能相关抗原（LFA-1; CD 11 a/CD 18）的表达。我们发现，与对照供体相比，疟疾患者的所有炎症和活化标志物的血浆水平显著增加。此外，我们发现了一种疾病诱导的T细胞耗竭与LFA-1抗原的高表达，特别是在CD 4（+）亚群。所获得的结果进一步支持了急性恶性疟原虫疟疾中T细胞重新分配至发炎内皮的假说。
To explain the observation that acute Plasmodium falciparum malaria is associated with a transient inability of peripheral blood cells to respond to antigenic stimulation in vitro, we have postulated the disease-induced reallocation of peripheral lymphocytes, possibly by adhesion to inflamed endothelium. We measured plasma levels of soluble markers of endothelial inflammation and T cell activation in 32 patients suffering from acute, uncomplicated P. falciparum malaria. as well as in 10 healthy, aparasitemic control donors. All donors were residents of a malaria-endemic area of Eastern State Sudan. In addition, we measured the T cell surface expression of the interleukin-2 receptor (CD25) and the lymphocyte function-associated antigen (LFA-1; CD11a/CD18). We found that the plasma levels of all inflammation and activation markers were significantly increased in the malaria patients compared with the control donors. In addition, we found a disease-induced depletion of T cells with high expression of the LFA-1 antigen, particularly in the CD4(+) subset. The results obtained provide further support for the hypothesis of T cell reallocation to inflamed endothelium in acute P. falciparum malaria.