Frequent reversible membrane damage in peripheral blood B cells in human T cell lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP)
Frequent reversible membrane damage in peripheral blood B cells in human T cell lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP)
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DOI：
10.1046/j.1365-2249.2000.01211.x
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发表时间：
2000-05-01
影响因子：
4.6
通讯作者：
Osame, M
中科院分区：
文献类型：
--
作者：
Furukawa, Y;Bangham, CRM;Osame, M
通过检测HTLV-I感染者体内外周血淋巴细胞的凋亡，研究HTLV-I感染时淋巴细胞的动态变化。新鲜分离的淋巴细胞从10个未感染的健康人，8个无症状的HTLV-I携带者和15例HAM/TSP用FITC标记的膜联蛋白V染色，检测磷脂酰丝氨酸（PS）残留暴露在外质膜小叶作为细胞凋亡的早期标志物。非感染者、无症状携带者和HAM/TSP患者的CD 4（+）和CD 8（+）淋巴细胞中annexin V阳性率无显著差异，但在15例HAM/TSP患者中，12例（80%）的CD 19（+）淋巴细胞（B细胞）上用FITC-annexin V检测到PS暴露显著增加，而只有八分之二（25%）的无症状携带者和没有感染的健康人在B细胞上显示这种异常的PS暴露。HAM/TSP中B细胞的膜联蛋白V染色强度为中等，与晚期凋亡细胞的高膜联蛋白V染色不同。然而，膜联蛋白V阳性降低时，细胞被染色后24小时的文化，这表明，在HAM/TSP中的B细胞的中间PS暴露不是一个凋亡过程的结果，而是反映可逆的膜损伤。PS暴露的B细胞可能提供了凝血和炎症的场所，从而有助于HAM/TSP及其并发症的发病机制。
Apoptosis in peripheral blood lymphocyte populations in HTLV-I-infected people in vivo was examined, to study the lymphocyte dynamics in HTLV-I infection. Freshly isolated lymphocytes from 10 non-infected healthy people, eight asymptomatic HTLV-I carriers and 15 patients with HAM/TSP were stained with FITC-labelled annexin V to detect phosphatidylserine (PS) residue exposure at the outer plasma membrane leaflet as an early marker of apoptosis. There was no significant difference in annexin V positivity in CD4(+) and CD8(+) lymphocytes between non-infected subjects, asymptomatic carriers and HAM/TSP patients, but there was a greatly increased exposure of PS on CD19(+) lymphocytes (B cells) detected by FITC-annexin V in 12 out of 15 (80%) HAM/TSP patients, while only two out of eight (25%) asymptomatic carriers and none of the non-infected healthy people showed this aberrant PS exposure on B cells. The intensity of annexin V staining of B cells in HAM/TSP was intermediate, as distinct from the high annexin V staining on advanced apoptotic cells. However, annexin V positivity was decreased when the cells were stained after 24 h of culture, suggesting that the intermediate PS exposure on the B cell in HAM/TSP is not a consequence of an apoptotic process, but rather reflects reversible membrane damage. B cells with PS exposure in vivo might provide a site for coagulation and inflammation, and so contribute to the pathogenesis of HAM/TSP and its complications.