2009.09.04 – The Activation of the JAK2/STAT5 Pathway Is Commonly Involved in Signaling through the Human IL-5 Receptor

http://content.karger.com/produktedb/produkte.asp?doi=237712

International Archives of Allergy and Immunology

Vol. 114, Suppl. 1, 1997

Free Abstract Article (PDF 1869 KB)

Eosinophils in Allergy and Related Diseases.
Editor(s): Ishikawa T. (Kumamoto), Makino S. (Tochigi), Fukuda T. (Tochigi)

Eosinophils in Allergy and Related Diseases

The Activation of the JAK2/STAT5 Pathway Is Commonly Involved in Signaling through the Human IL-5 Receptor
Norihisa Ogataa, Yuji Kikuchia, Taku Kouroa, Masao Tomonagab, Kiyoshi Takatsua

aDepartment of Immunology, Institute of Medical Science, University of Tokyo, Tokyo,
bDepartment of Hematology, Atomic Disease Institute, Nagasaki University School of Medicine, Nagasaki, Japan

Address of Corresponding Author

Int Arch Allergy Immunol 1997;114 (Suppl. 1):24-27 (DOI: 10.1159/000237712)

Key Words

  • IL-5, human
  • Signal transduction
  • JAK/STAT pathway

Abstract

The JAK (Janus kinase) family of protein tyrosine kinases and the STATs (signal transducers and activators of transcription) have been shown to be activated in response to a number of cytokines and growth factors. In this study, we evaluated the activation of JAK/STAT pathway upon human interleukin-5 (hIL-5) stimulation of two different hIL-5-responsive cell lines, hIL-5 receptor alpha.gif-subunit (hIL·5Ralpha.gif) cDNA-transfected TF-1 (TF-h5Ralpha.gif) and butyric-acid-treated YY-1 (YY-Bu), and peripheral eosinophils. Immunoprecipitation and electrophoretic mobility shift analysis revealed that tyrosine phosphorylation of JAK2 and activation of ST AT 5 were induced upon stimulation with hIL-5 in all three cell types, while STAT1 activation was only observed in eosinophils. These results indicate that JAK2/STAT5 activation is a common JAK/ STAT pathway for hIL-5-mediated signal in these cells.

Copyright © 1997 S. Karger AG, Basel

Author Contacts

Correspondence to: Dr. Kiyoshi Takatsu, Department of Immunology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108 (Japan), Tel. 3 5449 5260, Fax 3 5449 5407

Article Information

Published online: September 04, 2009
Number of Print Pages : 4