Regulation of Apoptosis in Myeloid Cells by Interferon Consensus Sequence-Binding Protein

doi:10.1084/jem.190.3.411

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© The Rockefeller University Press, 0022-1007/1999/8/411/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 3, August 2, 1999 411-422

Original Article

Regulation of Apoptosis in Myeloid Cells by Interferon Consensus Sequence–Binding Protein

Lucia Gabriele^a, Jan Phung^a, Jon Fukumoto^a, David Segal^a, I-Ming Wang^b, Paraskevi Giannakakou^c, Nathalie A. Giese^a, Keiko Ozato^b, and Herbert C. Morse, III^a

^a From The Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases
^b The Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development
^c The Medicine Branch, Division of Clinical Sciences, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-0760
LIP, NIAID, Bldg. 7, Rm. 308, 7 Center Dr., MSC 0760, NIH, Bethesda, MD 20892-0760.301-402-0077301-435-6525

lgabriele{at}atlas.niaid.nih.gov

Mice with a null mutation of the gene encoding interferon consensussequence–binding protein (ICSBP) develop a disease withmarked expansion of granulocytes and macrophages that frequentlyprogresses to a fatal blast crisis, thus resembling human chronicmyelogenous leukemia (CML). One important feature of CML isdecreased responsiveness of myeloid cells to apoptotic stimuli.Here we show that myeloid cells from mice deficient in ICSBPexhibit reduced spontaneous apoptosis and a significant decreasein sensitivity to apoptosis induced by DNA damage. In contrast,apoptosis in thymocytes from ICSBP-deficient mice is unaffected.We also show that overexpression of ICSBP in the human U937monocytic cell line enhances the rate of spontaneous apoptosisand the sensitivity to apoptosis induced by etoposide, lipopolysaccharideplus ATP, or rapamycin. Programmed cell death induced by etoposidewas specifically blocked by peptides inhibitory for the caspase-1or caspase-3 subfamilies of caspases. Studies of proapoptoticgenes showed that cells overexpressing ICSBP have enhanced expressionof caspase-3 precursor protein. In addition, analyses of antiapoptoticgenes showed that overexpression of ICSBP results in decreasedexpression of Bcl-X_L. These data suggest that ICSBP modulatessurvival of myeloid cells by regulating expression of apoptosis-relatedgenes.

Key Words: apoptosis • caspase • chronic myelogenous leukemia • interferon • interferon consensus sequence–binding protein

1used in this paper: CHX, cycloheximide; CML, chronic myelogenousleukemia; FMK, fluoromethyl ketone; ICSBP, interferon consensussequence–binding protein; IRF, interferon regulatory factor;ISGF, IFN-stimulated gene factor; ISRE, interferon-stimulatedresponse element; RT, reverse transcriptase; STAT, signal transducerand activator of transcription; TUNEL, TdT-mediated dUTP-biotinnick-end labeling

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