The molecular mechanism in the development of pathogenic T-cell through HTLV-1 in HTLV-1-associated myelopathy(HAM)

HTLV-1相关性脊髓病（HAM）的发病机制是HTLV-1感染的CD 4 ^+ T细胞引发的超免疫反应，导致中枢神经系统的慢性炎症。在这项研究中，证明了HTLV-1 Tax通过HTLV-1感染的CD 4 ^+ CD 25 ^+ CCR ^4 + T细胞中T-bet的转录激活诱导炎性细胞因子IFN-γ的产生。这些结果提示HTLV-1感染诱导的IFN-γ产生细胞导致感染细胞的可塑性可能在HAM的发生和发病中起重要作用。

In HTLV-1 associated myelopathy(HAM), the pathogenesis is known as HTLV-1 infected CD4^+T-cells triggered hyper immune response, which leads to chronic inflammation of the central nervous system. In this study, it was demonstrated that HTLV-1 Tax induced the inflammatory cytokine IFN-γproduction through the transcriptional activation of T-bet in HTLV-1 infected CD4^+CD25^+CCR^4+T-cells. These results suggested that HTLV-1 infection-induced IFN-g producing cells resulting in plasticity of infected cells may play an important role in the development and pathogenesis of HAM.