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Prepublished online as a Blood First Edition Paper on August 14, 2003; DOI 10.1182/blood-2003-04-1043.
Submitted April 3, 2003
Accepted August 4, 2003
Activation of interleukin-13 expression in T cells from HTLV-1-infected individuals and in chronically infected cell lines
Hye-Kyung Chung, Howard A Young, Peter K C Goon, Gisela Heidecker, Gerald L Princler, Osamu Shimozato, Graham P Taylor, Charles R M Bangham, and David Derse*
Basic Research Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD, USA
Laboratory of Experimental Immunology, National Cancer Institute, National Institutes of Health, Frederick, MD, USA
Department of Immunology, Imperial College School of Medicine, London, United Kingdom
Department of Genito-Urinary Medicine and Communicable Diseases, Imperial College School of Medicine, London, United Kingdom
* Corresponding author; email: derse{at}ncifcrf.gov.
Human T-cell leukemia virus type 1 (HTLV-1) infection profoundly alters T-cell gene expression and the dysregulated synthesis of cytokines could influence the course and pathological consequences of infection. In the process of screening T-cell lines for Th1 and Th2 cytokine mRNAs, we observed that IL-13 mRNA was highly expressed in HTLV-1 infected, IL-2 dependent T-cell lines. IL-9 and interferon gamma (IFN- ) mRNAs were also expressed at high levels in chronically infected cell lines. IL-5 mRNA was detected in 60% of the HTLV-1 infected cell lines, but mRNAs for IL-4, IL-10, IL-2, and IL-15 were either below detection limits or did not correlate with HTLV-1 infection. Transcriptional activation of the IL-13 promoter by the HTLV-1 Tax trans-regulatory protein was demonstrated in Jurkat T-cells transiently transfected with an Il-13 promoter-reporter plasmid. The clinical relevance of these observations was demonstrated by immunofluorescent staining and flow cytometry of lymphocytes obtained from HTLV-1 infected patients. These studies revealed that IL-13 production was directly related to the level of Tax expression in the infected CD4+ T-cells soon after in vitro culture. As IL-13 plays key roles in tumor immuno-surveillance, asthma, and central nervous system inflammation, it may contribute to the pathophysiology of HTLV-1 associated diseases.
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