GD2 GANGLIOSIDE ON HUMAN T-LYMPHOTROPIC VIRUS TYPE-I-INFECTED T-CELLS - POSSIBLE ACTIVATION OF BETA-1,4-N-ACETYLGALACTOSAMINYLTRANSFERASE GENE BY P40(TAX)
GD2 GANGLIOSIDE ON HUMAN T-LYMPHOTROPIC VIRUS TYPE-I-INFECTED T-CELLS - POSSIBLE ACTIVATION OF BETA-1,4-N-ACETYLGALACTOSAMINYLTRANSFERASE GENE BY P40(TAX)
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DOI：
10.1073/pnas.90.5.1972
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发表时间：
1993-03-01
影响因子：
11.1
通讯作者：
FURUKAWA, K
中科院分区：
文献类型：
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作者：
FURUKAWA, K;AKAGI, T;FURUKAWA, K
利用一组单克隆抗体测定了神经节苷脂在成人T细胞白血病（ATL）和人T细胞白血病病毒I型（HTLV - I）感染细胞上的表达。ATL细胞系和HTLV - I感染细胞特异性表达GD2。ATL患者的白血病细胞通常低水平表达GD2，但在白细胞介素2存在下体外培养约一周后，GD2⁺细胞的百分比增加至40 - 70%。在相同条件下体外培养时，其他类型的白血病细胞和正常外周T细胞不表达GD2。培养的ATL细胞中GD2的出现与HTLV - 1基因产物p40tax的表达相对应。与仅含新霉素抗性基因的对照淋巴细胞相比，感染表达p40tax的逆转录病毒载体的外周淋巴细胞高水平表达GD2。通过逆转录 - 聚合酶链反应分析证明这些细胞中β - 1,4 - N - 乙酰半乳糖胺基转移酶（GM2 / GD2合酶）mRNA水平明显升高。在未培养的ATL细胞中也观察到HTLV - I tax1 / rex1基因的mRNA表达与β - 1,4 - N - 乙酰半乳糖胺基转移酶基因之间的一致性。这些结果表明，GD2的高表达是由于在体外和体内p40tax诱导该酶表达增加，从而由前体GD3新合成所致。
Ganglioside expression on adult T-cell leukemia (ATL) and human T-cell lymphotropic virus type I (HTLV-I)-infected cells was determined by using a panel of monoclonal antibodies. ATL lines and HTLV-1-infected cells specifically expressed GD2. Leukemia cells from ATL patients generally expressed low levels of GD2 but the percentage of GD2+ cells increased up to 40-70% after in vitro culture in the presence of interleukin 2 for about a week. No other type of leukemia cells and normal peripheral T cells expressed GD2 during in vitro culture under the same conditions. The appearance of GD2 in the cultured ATL cells corresponded with the expression of p40tax, a product of the HTLV-1 gene. Peripheral lymphocytes infected with a p40tax-expressing retroviral vector expressed high levels of GD2 in comparison with control lymphocytes containing the neomycin-resistance gene alone. The apparently increased levels of beta-1,4-N-acetylgalactosaminyltransferase (GM2/GD2 synthase) mRNA in these cells were demonstrated by reverse transcription-polymerase chain reaction analysis. Concordance between mRNA expression for the HTLV-I tax1/rex1 genes and the beta-1,4-N-acetylgalactosaminyltransferase gene was also observed in uncultured ATL cells. These results suggest that high GD2 expression was due to neosynthesis from precursor GD3 by increased expression of this enzyme induced by p40tax in vitro and in vivo.