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1. Relationship of the clinical response and binding of recombinant interferon alpha in patients with lymphoproliferative diseases

Author

Faltynek, CR, Princler, GL, Rossio, JL, Ruscetti, FW, Maluish, AE, Abrams, PG, and Foon, KA

Abstract

Patients with hairy cell leukemia (HCL) and chronic lymphocytic leukemia (CLL) were treated with recombinant interferon alpha A (rIFN- alpha A). The binding of iodinated recombinant interferon-alpha to baseline samples of peripheral blood mononuclear cells (PBMCs) from the leukemia patients was compared with clinical responsiveness to rIFN- alpha A. HCL patients (8/10) responded to rIFN-alpha A therapy, whereas none (0/10) of the CLL patients studied responded. The PBMCs from the eight responsive HCL patients bound approximately twice as much iodinated interferon as the PBMCs from nonresponsive CLL patients. This difference was due to more high-affinity receptors per cell with no difference in the affinity of the interferon-receptor interaction. However, because PBMCs from HCL patients were larger than PBMCs from CLL patients, the cell surface receptor density was similar. The leukemic cells from one of the two nonresponsive HCL patients bound iodinated interferon similarly to the cells from the responsive HCL patients, whereas the leukemic cells from the other nonresponsive HCL patient bound considerably less. The rapidity of response of the HCL patients did not correlate with the level of binding of iodinated interferon. Our results suggest that the absolute number of interferon receptors per cell may be only one of several important parameters in the response to rIFN-alpha A therapy, and that the responsiveness of a particular lymphoproliferative disease or a particular patient to rIFN- alpha A therapy cannot be predicted or explained solely by the degree of interaction between IFN and its cell surface receptor.

Published
1986
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2. Activation of interleukin-13 expression in T cells from HTLV-1-infected individuals and in chronically infected cell lines.

Author

Chung HK, Young HA, Goon PK, Heidecker G, Princler GL, Shimozato O, Taylor GP, Bangham CR, and Derse D

Subjects
Case-Control Studies, Cell Line, Transformed, Cytokines biosynthesis, Cytokines genetics, Gene Products, tax genetics, Gene Products, tax physiology, Humans, Interferon-gamma biosynthesis, Interferon-gamma genetics, Interleukin-13 genetics, Interleukin-5 biosynthesis, Interleukin-5 genetics, Interleukin-9 biosynthesis, Interleukin-9 genetics, Jurkat Cells, Promoter Regions, Genetic, RNA, Messenger analysis, T-Lymphocytes metabolism, Transduction, Genetic, HTLV-I Infections pathology, Interleukin-13 biosynthesis, T-Lymphocytes virology, Transcriptional Activation
Abstract

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 pathologic consequences of infection. In the process of screening T-cell lines for T helper 1 (Th1) and Th2 cytokine mRNAs, we observed that interleukin-13 (IL-13) mRNA was highly expressed in HTLV-1-infected, IL-2-dependent T-cell lines. IL-9 and interferon gamma (IFN-gamma) 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 immunosurveillance, asthma, and central nervous system inflammation, it may contribute to the pathophysiology of HTLV-1-associated diseases.

Published
2003
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