共查询到20条相似文献,搜索用时 625 毫秒
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
Novel blocker of NFAT activation inhibits IL-6 production in human myometrial arteries and reduces vascular smooth muscle cell proliferation 总被引:1,自引:0,他引:1
Nilsson LM Sun ZW Nilsson J Nordström I Chen YW Molkentin JD Wide-Swensson D Hellstrand P Lydrup ML Gomez MF 《American journal of physiology. Cell physiology》2007,292(3):C1167-C1178
12.
13.
Aberrant activation of the interleukin-2 autocrine loop through the nuclear factor of activated T cells by nonleukemogenic human T-cell leukemia virus type 2 but not by leukemogenic type 1 virus 下载免费PDF全文
Niinuma A Higuchi M Takahashi M Oie M Tanaka Y Gejyo F Tanaka N Sugamura K Xie L Green PL Fujii M 《Journal of virology》2005,79(18):11925-11934
Human T-cell leukemia virus type 1 (HTLV-1) but not HTLV-2 is associated with adult T-cell leukemia. We found that HTLV-2 Tax2 protein stimulated reporter gene expression regulated by the interleukin (IL)-2 promoter through the nuclear factor of activated T cells (NFAT) in a human T-cell line (Jurkat). However, the activity of HTLV-1 Tax1 was minimal in this system. T-cell lines immortalized by HTLV-2 but not HTLV-1 constitutively exhibited activated NFAT in the nucleus and constitutively expressed IL-2 mRNA. Cyclosporine A, an inhibitor of NFAT activation, abrogated the induction of IL-2 mRNA in HTLV-2-immortalized T-cell lines and concomitantly inhibited cell growth. This growth inhibition was rescued by the addition of IL-2 to the culture. Furthermore, anti-IL-2 receptor antibodies significantly reduced the proliferation of HTLV-2-infected T-cell lines but not that of HTLV-1-infected cells. Our results suggest that Tax2 activates an IL-2 autocrine loop mediated through NFAT that supports the growth of HTLV-2-infected cells under low-IL-2 conditions. This mechanism would be especially important in vivo, where this autocrine mechanism establishes a nonleukemogenic life-long HTLV-2 infection. The results also suggest that differences in long-term cytokine production between HTLV-1 and HTLV-2 infection are another factor for the differences in pathogenesis. 相似文献
14.
15.
16.
17.
18.
19.