The Tax protein of the HTLV-l retrovirus, which causes an aggressive form of T cell leukaemia known as adult T cell leukaemia (ATL), upregulates the expression of various cytokines known to be produced by infected cells by methods similar to CD28 costimulation (the target sites are the same). T cell proliferation and expansion are aided by certain of these cytokines, particularly IL-2. Although it is unclear how this contributes to the development of leukaemia, Tax transactivation of cellular gene expression is critical to its ability to convert cells. In Jurkat Leukemia T cells transiently transfected for producing the Tax protein, on the other hand, all-trans-retinoic acid (ATRA) reduces JNK-1 activity, antagonising the action of the Tax protein. The decrease in JNK-1 activity was accompanied by a significant drop in the expression of IL-2 and IFN- in Jurkat cells treated with ATRA in a dose-dependent manner, implying a link between JNK-1 expression and Tax protein function. The ATRA therapy was unable to reduce IL-4 and IL-10 expression. Both AP-1 and NF-B were influenced by ATRA therapy, according to a luciferase experiment using a well-known reporter gene expressing the IL-2 promoter or a tandem repeat of AP-1 or NF-B. Furthermore, our findings revealed that JNK-1 is constitutively activated in Jurkat Leukemia T cells expressing the Tax protein, implying that JNK-1 is essential for Jurkat leukaemia cell proliferation triggered by Tax.
Author(S) Details
Eduardo Parra Villegas
Biomedical Experimental Laboratory, School of Medicine, University of Tarapaca. Avenida Senador Luis Valente Rossi, Arica, Chile.
Pedro Hecht López
Biomedical Experimental Laboratory, School of Medicine, University of Tarapaca. Avenida Senador Luis Valente Rossi, Arica, Chile.
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