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Volume 272, Number 9, Issue of February 28, 1997 pp. 5487-5494
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

Tumor Necrosis Factor alpha  Enhances the Expression of the Interleukin (IL)-4 Receptor alpha -Chain on Endothelial Cells Increasing IL-4 or IL-13-induced Stat6 Activation

(Received for publication, September 30, 1996)

Serena M. Lugli , Ningping Feng § , Markus H. Heim , Michèle Adam , Bruno Schnyder par , Hansueli Etter , Mat Yamage , Hans-Pietro Eugster , Rudolf A. Lutz § , Gerard Zurawski ** and René Moser

From the Institute of Toxicology, Federal Institute of Technology, CH-8057 Zurich, § Institute of Clinical Chemistry, University Hospital, CH-8091 Zurich,  Department of Research, University Hospital, CH-4031 Basel, Switzerland, par  Dupont Merck Pharmaceutical Co., Stine-Haskell Research Center, Newark, Delaware 19714, and ** DNAX Research Institute of Cellular and Molecular Biology, Palo Alto, California 94304

Functional receptors for interleukin (IL)-4 and IL-13 on endothelial cells consist of the 130-kDa IL-4 receptor alpha -chain (IL-4Ralpha ) and a 65-75-kDa IL-13 binding subunit that are expressed in a ratio of about 1:3, respectively. The restricted number of IL-4Ralpha limits subunit heterodimerization and in turn receptor-mediated signaling. We report here, the effects of tumor necrosis factor alpha  (TNF-alpha ) on the expression of the receptor subunits for IL-4 and IL-13. By flow cytofluorometry and receptor-binding analysis of iodinated IL-4 and IL-13, stimulation with TNF-alpha -induced a 2-3-fold increase of the IL-4Ralpha expression. The up-regulation was also confirmed at the transcriptional level by reverse transcription-polymerase chain reaction. Radioligand cross-linking experiments revealed no change in the subunit composition of the TNF-alpha -induced receptor complex. Nevertheless, TNF-alpha stimulation led to increased activation of the IL-4-specific signal transducers and activators of transcription protein (Stat6) by IL-4 and IL-13. Thus, TNF-alpha corrects the subunit imbalance of the endothelial IL-4·IL-13 receptor complex thereby increasing receptor heterodimerization and in turn the signaling capability by IL-4 and IL-13.


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