Eggena Mark P, Hopkins Heidi, Barugahare Banson, Okello Martin, Ssali Francis, Mugyenyi Peter, Rosenthal Philip J, Cao Huyen, Dorsey Grant
Department of Medicine, San Francisco General Hospital, University of California, San Francisco, California, USA.
Am J Trop Med Hyg. 2006 Jan;74(1):41-3.
Host immunity plays an important role in response to antimalarial therapy but is poorly understood. To test whether T cell activation is a risk factor for antimalarial treatment failure, we studied CD4(+) and CD8(+) T cell activation in 31 human immunodeficiency virus-negative Ugandan patients 5-37 years of age who were treated for uncomplicated Plasmodium falciparum malaria. Increased CD4(+) T cell activation, as indicated by co-expression of HLA-DR and CD38, was an independent risk factor for treatment failure (hazard ratio = 2.45, 95% confidence interval = 1.02-5.89, P = 0.05) in multivariate analysis controlling for age, baseline temperature, and pre-treatment parasite density. The results provide insight into the role of cellular immunity in response to antimalarial therapy and underscore the need to investigate the mechanisms behind immune activation.
宿主免疫在对抗疟疾治疗的反应中起着重要作用，但目前人们对此了解甚少。为了测试T细胞活化是否是抗疟疾治疗失败的一个风险因素，我们研究了31名年龄在5至37岁的乌干达人类免疫缺陷病毒阴性患者的CD4(+)和CD8(+)T细胞活化情况，这些患者因非复杂性恶性疟原虫疟疾接受治疗。在控制年龄、基线体温和治疗前寄生虫密度的多变量分析中，如通过HLA-DR和CD38共表达所表明的，CD4(+)T细胞活化增加是治疗失败的一个独立风险因素（风险比=2.45，95%置信区间=1.02-5.89，P=0.05）。这些结果为细胞免疫在对抗疟疾治疗反应中的作用提供了见解，并强调了研究免疫激活背后机制的必要性。
