Abstract

Human T-cell leukemia/lymphoma virus type 1 (HTLV-1) induces aberrant nuclear factor-κB (NF-κB) activation. Although Tax is thought to play major roles in NF-κB activation, cells expressing Tax become a target of cytotoxic T cells. Accordingly, HTLV-1–infected cells lose Tax expression and acquire Tax-independent NF-κB activation. Blocking NF-κB 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-κB appears to be the common biological basis shared between HTLV-1–infected untransformed cells and ATL cells, blocking NF-κB might be a potential strategy for treating and preventing ATL.

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