CONSTITUTIVELY ACTIVATED JAK-STAT PATHWAY IN T-CELLS TRANSFORMED WITH HTLV-I

被引:504
作者
MIGONE, TS
LIN, JX
CERESETO, A
MULLOY, JC
O'SHEA, JJ
FRANCHINI, G
LEONARD, WJ
机构
[1] NHLBI, MOLEC IMMUNOL LAB, BETHESDA, MD 20892 USA
[2] NCI, TUMOR CELL BIOL LAB, BETHESDA, MD 20892 USA
[3] NIAMSD, ARTHRITIS & RHEUMATISM BRANCH, BETHESDA, MD 20892 USA
关键词
D O I
10.1126/science.7604283
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Human T cell lymphotropic virus I (HTLV-I) is the etiological agent for adult T cell leukemia and tropical spastic paraparesis (also termed HTLV-I-associated myelopathy). HTLV-I-infected peripheral blood T cells exhibit an initial phase of interleukin-2 (IL-2)-dependent growth; over time, by an un known mechanism, the cells become IL-2-independent. Whereas the Jak kinases Jak1 and Jak3 and the signal transducer and activator of transcription proteins Stat3 and Stat5 are activated in normal T cells in response to IL-2, this signaling pathway was constitutively activated in HTLV-I-transformed cells. In HTLV-I-infected cord blood lymphocytes, the transition from IL-2-dependent to IL-2-independent growth correlated with the acquisition of a constitutively activated Jak-STAT pathway, which suggests that this pathway participates in HTLV-I-mediated T cell transformation.
引用
收藏
页码:79 / 81
页数:3
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