细胞间黏附分子-3（ICAM-3）独立于树突状细胞特异性细胞间黏附分子-3抓取非整合素（DC-SIGN）介导的传播，影响1型人类免疫缺陷病毒在CD4(+) T细胞中的复制。
ICAM-3 influences human immunodeficiency virus type 1 replication in CD4(+) T cells independent of DC-SIGN-mediated transmission.
作者信息
Biggins Julia E, Biesinger Tasha, Yu Kimata Monica T, Arora Reetakshi, Kimata Jason T
机构信息
Department of Molecular Virology and Microbiology, BCM385, Room 811D, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
出版信息
Virology. 2007 Aug 1;364(2):383-94. doi: 10.1016/j.virol.2007.03.017. Epub 2007 Apr 16.
We investigated the role of ICAM-3 in DC-SIGN-mediated human immunodeficiency virus (HIV) infection of CD4(+) T cells. Our results demonstrate that ICAM-3 does not appear to play a role in DC-SIGN-mediated infection of CD4(+) T cells as virus is transmitted equally to ICAM-3(+) or ICAM-3(-) Jurkat T cells. However, HIV-1 replication is enhanced in ICAM-3(-) cells, suggesting that ICAM-3 may limit HIV-1 replication. Similar results were obtained when SIV replication was examined in ICAM-3(+) and ICAM-3(-) CEMx174 cells. Furthermore, while ICAM-3 has been proposed to play a co-stimulatory role in T cell activation, DC-SIGN expression on antigen presenting cells did not enhance antigen-dependent activation of T cells. Together, these data indicate that while ICAM-3 may influence HIV-1 replication, it does so independent of DC-SIGN-mediated virus transmission or activation of CD4(+) T cells.
我们研究了细胞间黏附分子3（ICAM-3）在树突状细胞特异性细胞间黏附分子3抓取非整合素（DC-SIGN）介导的人类免疫缺陷病毒（HIV）感染CD4(+) T细胞过程中的作用。我们的结果表明，ICAM-3似乎在DC-SIGN介导的CD4(+) T细胞感染中不起作用，因为病毒同等程度地传播至ICAM-3(+)或ICAM-3(-)的人急性T淋巴细胞白血病细胞（Jurkat T细胞）。然而，HIV-1在ICAM-3(-)细胞中的复制增强，这表明ICAM-3可能限制HIV-1复制。在ICAM-3(+)和ICAM-3(-)的人T淋巴细胞白血病细胞系（CEMx174细胞）中检测猴免疫缺陷病毒（SIV）复制时，也获得了类似结果。此外，虽然有人提出ICAM-3在T细胞活化中起共刺激作用，但抗原呈递细胞上DC-SIGN的表达并未增强T细胞的抗原依赖性活化。总之，这些数据表明，虽然ICAM-3可能影响HIV-1复制，但其作用独立于DC-SIGN介导的病毒传播或CD4(+) T细胞的活化。
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