HIV-1 NL4-3, but not IIIB, inhibits JAK3/STAT5 activation in CD4(+) T cells.
HIV-1 NL4-3, but not IIIB, inhibits JAK3/STAT5 activation in CD4(+) T cells.
复制标题
HIV-1 NL4-3（而非 IIIB）抑制 CD4(+) T 细胞中 JAK3/STAT5 的激活。
DOI：
10.1006/viro.2001.0994
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发表时间：
2001
期刊：
影响因子：
3.7
通讯作者：
Finkel,TH
中科院分区：
文献类型：
--
作者：
Selliah,N;Finkel,TH
HIV-1感染导致体内和体外T细胞功能障碍和凋亡。IL-2 R的共有γ链及其相关的Janus激酶JAK 3对于正常T细胞功能和存活是必不可少的。我们已经报道了CD 4与HIV gp 120的连接抑制T细胞受体诱导的JAK 3的活化和表达。我们还表明，虽然一些HIV-1毒株，如NL 4 -3，诱导受感染的CD 4 +T细胞凋亡，但其他毒株，如HIV-1 IIIB，则不会。有趣的是，我们在这里显示，用HIV-1 NL 4 -3感染CD 4 +T细胞，而不是IIIB，抑制JAK 3的活化和表达。NL 4 -3感染的T细胞在通过TCR/CD 3刺激后不能上调JAK 3表达。此外，NL 4 -3，而不是IIIB，抑制酪氨酸磷酸化和STAT 5的表达，JAK 3的下游目标。这些数据表明HIV-1感染的T细胞的凋亡与JAK 3/STAT 5活化途径的抑制之间存在相关性。
HIV-1 infection leads to T cell dysfunction and apoptosis in vivo and in vitro. The shared common γ chain of IL-2R and its associated Janus kinase, JAK3, are indispensable for normal T cell function and survival. We have reported that CD4 ligation with HIV gp120 inhibits T cell receptor-induced activation and expression of JAK3. We have also shown that while some strains of HIV-1, such as NL4-3, induce apoptosis of infected CD4+T cells, other strains, such as HIV-1 IIIB, do not. Interestingly, we show here that infection of CD4+T cells with HIV-1 NL4-3, but not IIIB, inhibited activation and expression of JAK3. NL4-3-infected T cells were unable to upregulate JAK3 expression following stimulation through TCR/CD3. In addition, NL4-3, but not IIIB, inhibited tyrosine phosphorylation and expression of STAT5, a downstream target of JAK3. These data suggest a correlation between apoptosis of HIV-1-infected T cells and inhibition of the JAK3/STAT5 activation pathway.