Horie Ryouichi
Department of Hematology, School of Medicine, Kitasato University, 1-15-1 Kitasato, Sagamihara, Kanagawa 228-8555, Japan.
Int Rev Immunol. 2007 Sep-Dec;26(5-6):269-81. doi: 10.1080/08830180701703364.
Human T-cell leukemia/lymphoma virus type 1 (HTLV-1) induces aberrant nuclear factor-kappaB (NF-kappaB) activation. Although Tax is thought to play major roles in NF-kappaB activation, cells expressing Tax become a target of cytotoxic T cells. Accordingly, HTLV-1-infected cells lose Tax expression and acquire Tax-independent NF-kappaB activation. Blocking NF-kappaB not only induces apoptosis in adult T-cell leukemia/lymphoma (ATL) cells but also reduces the number of HTLV-1-infected cells in virus carriers. Therefore, because constitutively activated NF-kappaB appears to be the common biological basis shared between HTLV-1-infected untransformed cells and ATL cells, blocking NF-kappaB might be a potential strategy for treating and preventing ATL.
人类T细胞白血病/淋巴瘤病毒1型（HTLV-1）可诱导核因子-κB（NF-κB）异常激活。尽管Tax被认为在NF-κB激活中起主要作用，但表达Tax的细胞会成为细胞毒性T细胞的靶标。因此，HTLV-1感染的细胞会失去Tax表达，并获得不依赖Tax的NF-κB激活。阻断NF-κB不仅可诱导成人T细胞白血病/淋巴瘤（ATL）细胞凋亡，还可减少病毒携带者中HTLV-1感染细胞的数量。因此，由于持续激活的NF-κB似乎是HTLV-1感染的未转化细胞和ATL细胞共有的共同生物学基础，阻断NF-κB可能是治疗和预防ATL的潜在策略。
