Authors: Daniel Myrtek; Mathias Knoll¹; Timm Matthiesen¹; Sebastian Krause²; Jens Lohrmann³; Dirk Schillinger³; Marco Idzko¹; J. Christian Virchow⁴; Karlheinz Friedrich²; Werner Luttmann⁴

Source: Immunology, Volume 112, Number 4, August 2004 , pp. 597-604(8)

Publisher: Wiley-Blackwell

Abstract:

Summary

Interleukin-13 (IL-13) is critical for the development of allergic asthma and is involved in the activation of eosinophils within the airways. IL-13 exerts its activity on target cells via the dimeric IL-13 receptor (IL-13R), which comprises the IL-13 receptor 1-chain (IL-13R1) as a specific component. The aim of this study was to investigate the expression of the IL-13R1-chain on primary human eosinophilic granulocytes. Furthermore, it addresses the regulatory influence of cytokines on the level of surface abundance of this receptor subunit. Expression of IL-13- and IL-4-receptor subunits in purified primary human eosinophils was monitored at the messenger RNA level by reverse transcription polymerase chain reaction and at the protein level by flow cytometry. For the analysis of IL-13R1 surface expression, a new monoclonal antibody, which was generated using genetic immunization, was employed. Different cytokines with established activity on eosinophils were studied with regard to their influence on IL-13R1 in vitro by flow cytometry. Whereas IL-13 and IL-4 had inhibitory effects on IL-13R1 expression on eosinophils, interferon-, tumour necrosis factor-, and, to the largest extent, transforming growth factor-, enhanced the expression of this receptor subunit. A positive regulatory response evoked by transforming growth factor- and interferon- does not prevent inhibitory effects caused by IL-13. These findings suggest a regulatory cytokine network influencing the reactivity of eosinophils to IL-13.

Keywords: asthma; IL-13 receptor; surface expression; transforming growth factor-

Document Type: Research article

DOI: http://dx.doi.org/10.1046/j.1365-2567.2004.01897.x

Affiliations: 1: Department of Pneumology, University Hospital Freiburg, Freiburg, Germany 2: Institute of Biochemistry I, Friedrich Schiller University of Jena Medical School, Jena, Germany 3: GENOVAC AG, Freiburg, Germany 4: Department of Pneumology, University Hospital Rostock, Rostock, Germany

Publication date: 2004-08-01

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