Tax protein of HTLV-1 activates the transcriptional capacity of the NF-κB family, resulting in up-regulation of various genes, which are linked to phenotypic alterations of HTLV-1-infected T cells. To understand NF-κB regulation in HTLV-1-infected leukemic cells in vivo, we analyzed expression of NF-κB and IκB in primary cells isolated from ATL patients. Using competitive polymerase chain reaction, we observed an elevated expression of IκB mRNA in all four ATL cases tested. In contrast to the elevated mRNA levels, the levels of IκB protein were remarkably reduced in some of these cases, suggesting destabilization of IκB protein. On the other hand, mRNA expression of p50/p105 and p65, subfamilies of NF-κB, was enhanced in primary cells isolated from some ATL patients. Furthermore, the expression patterns of NF-κB subfamily were variable among patients and also different from those in T cells isolated from uninfected individuals. Although the number of cases analyzed was limited, we can conclude from these observations that activation of NF-κB is restricted to a few subfamilies in vivo. These findings in vivo are strikingly different from those in HTLV-1-infected T cell lines in vitro, in which Tax is responsible for NF-κB activation. It is therefore suggested that the elevation of NF-κB expression in leukemic cells of ATL patients might not be supported mainly by the viral protein Tax.