Elhassan I M, Hviid L, Satti G, Akerstrom B, Jakobsen P H, Jensen J B, Theander T G
Department of Infectious Diseases, University Hospital (Rigshospitalet), Copenhagen, Denmark.
Am J Trop Med Hyg. 1994 Sep;51(3):372-9. doi: 10.4269/ajtmh.1994.51.372.
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, uncomplication 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.
为了解释急性恶性疟原虫疟疾与外周血细胞在体外暂时无法对抗抗原刺激这一观察结果，我们推测疾病诱导外周淋巴细胞重新分布，可能是通过黏附于炎症内皮细胞。我们测量了32例患有急性、无并发症恶性疟原虫疟疾患者以及10例健康、无寄生虫血症对照者血浆中内皮炎症和T细胞活化的可溶性标志物水平。所有供者均为苏丹东部州疟疾流行地区的居民。此外，我们还测量了白细胞介素-2受体（CD25）和淋巴细胞功能相关抗原（LFA-1；CD11a/CD18）的T细胞表面表达。我们发现，与对照供者相比，疟疾患者所有炎症和活化标志物的血浆水平均显著升高。此外，我们发现疾病诱导高表达LFA-1抗原的T细胞减少，尤其是在CD4+亚群中。所得结果为急性恶性疟原虫疟疾中T细胞重新分布至炎症内皮细胞的假说提供了进一步支持。
