Role of incidental and/or cured intestinal parasitic infections on profile of CD4+ and CD8+ T cell subsets and activation status in HIV-1 infected and uninfected adult Ethiopians
Role of incidental and/or cured intestinal parasitic infections on profile of CD4+ and CD8+ T cell subsets and activation status in HIV-1 infected and uninfected adult Ethiopians
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DOI：
10.1046/j.1365-2249.2003.02106.x
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发表时间：
2003-04-01
影响因子：
4.6
通讯作者：
De Wit, TFR
中科院分区：
文献类型：
--
作者：
Kassu, A;Tsegaye, A;De Wit, TFR
肠道寄生虫感染被认为会引起持续的免疫激活，导致免疫状态不平衡。这种状态被认为是非洲艾滋病发病的一个主要因素。本研究调查了偶发寄生虫感染和治疗对来自HIV-1感染和未感染的埃塞俄比亚成年人的T细胞分化和CD4（+）和CD8(+) T细胞激活标记物的影响。来自64名受试者（41名hiv阴性和23名hiv阳性）的冷冻保存pbmc，每隔6个月随访一次，用于比较偶然肠道寄生虫及其治疗对T细胞亚群特征和激活状态的影响。样品用各种T细胞分化和激活标记物的抗体染色，允许通过三色FACScan对初始、记忆、效应、记忆/效应、激活和静息CD4（+）和CD8(+) T细胞亚群进行量化。偶发肠道寄生虫感染导致hiv阴性和hiv阳性受试者的记忆CD4(+) T细胞数量显著增加（P < 0.05）。与寄生虫共感染的hiv阳性人群中，CD8(+) HLA-DR+ T细胞比例也显著升高（P < 0.05）。在hiv阴性受试者中，寄生虫治疗后活化细胞显著减少，静息CD8(+) T细胞显著增加（P < 0.05）。这些数据表明，肠道寄生虫感染可能导致T细胞亚群计数的改变，也可能导致外周血T细胞活化标志物的上调。寄生虫感染的治疗显示出降低激活的趋势，这表明，与其他基于社区的干预策略一起，这种治疗可以用来下调免疫激活，从而保护宿主不容易受到艾滋病毒的攻击。
Intestinal parasitic infections have been suggested to cause persistent immune activation leading to an unbalanced immune state. Such a state has been proposed to be a major factor in the pathogenesis of AIDS in an African context. The present study investigated the effect of incidental parasitic infection and treatment on the profile of T cell differentiation and activation markers on CD4(+) and CD8(+) T cells from HIV-1 infected and uninfected adult Ethiopians. Cryopreserved PBMCs from 64 subjects (41 HIV-negative and 23 HIV-positive) with follow-up visits at 6-monthly intervals were used to compare the effect of incidental intestinal parasites and their treatment upon T cell subset profiles and activation status. The samples were stained with antibodies to various T cell differentiation and activation markers allowing naive, memory, effector, memory/effector, activated and resting CD4(+) and CD8(+) T cell subsets to be quantified by triple-colour FACScan. Incidental intestinal parasitic infections resulted in a significant increase in memory CD4(+) T cell numbers both in HIV-negative and HIV-positive subjects (P < 0.05). There was also a significant increase in the percentage of CD8(+) HLA-DR+ T cells (P < 0.05) in HIV-positive subjects co-infected with parasites. In HIV-negative subjects, a significant decline in activated cells and a significant increase in resting CD8(+) T cells (P < 0.05) was observed after treatment for parasites. These data suggest that intestinal parasitic infections could result in the alteration of T cell subset counts and also in the up-regulation of T cell activation markers in peripheral blood. Treatment of parasitic infections showed a tendency to reduce the activation suggesting that, together with other community based intervention strategies, such treatment could be used to down-regulate immune activation and hence protect the host from being easily attacked by HIV.