Transactivation of the Interleukin - la Promoter by Human T - cel l Leukemia Virus Type I and Type I 1 Tax Proteins

Human T-cell leukemia virus type I (HTLV-1)-infected T-cell lines constitutively produce high levels of interleukin-la (ILla). To analyze the mechanisms that lead t o the expression of ILla in HTLV-I-infected cell lines, we studied regulatory regions of the human IL-la promoter involved in activation of the IL-la gene. IL-la promoter constructs drive transcription of the chloramphenicol acetyltransferase (CAT) reporter gene in HTLV-I-positive MT-2 cells, which constitutively produce IL-la. In a cotransfection assay, the Tax protein of both HTLV-I and HTLV-II specifically activated transcription from the IL-la promoter in an uninfected Jurkat cell line. A mutant Tax protein deficient in transactivation of genes by the nuclear factor (NFI-KB pathway was unable to induce transcriptional activity of IL-la promoter-CAT constructs, but was rescued by exogenous provision of ~ 6 5 1 ~ 5 0 NF-KB. We