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J Biol Chem, Vol. 273, Issue 37, 24016-24024, September 11, 1998

Molecular Analysis of Human Interleukin-9 Receptor Transcripts in Peripheral Blood Mononuclear Cells
IDENTIFICATION OF A SPLICE VARIANT ENCODING FOR A NONFUNCTIONAL CELL SURFACE RECEPTOR

Luigi Grasso, Minxue Huang, Christine D. Sullivan, Carol J. Messler, Matt B. Kiser, Carl R. Dragwa, Kenneth J. Holroyd, Jean-Christophe Renauld, Roy C. Levitt, and Nicholas C. Nicolaides

From the Magainin Institute of Molecular Medicine, Magainin Pharmaceuticals, Inc., Plymouth Meeting, Pennsylvania 19462 and  Ludwig Institute for Cancer Research and Experimental Medicine Unit, University of Louvain, Avenue Hippocrate, B-1200 Brussels, Belgium

Genetic studies on mouse models of asthma have identified interleukin-9 (IL9) as a determining factor in controlling bronchial hyperresponsiveness, a hallmark of the disease. Recently, the human IL9 receptor (hIL9R) gene locus has also been implicated in determining susceptibility to bronchial hyperresponsiveness and asthma. In order to evaluate the structure and function of the encoded product, we analyzed receptor transcripts derived from peripheral blood mononuclear cells of 50 unrelated donors. Sequence analysis of the entire coding region identified a splice variant that contains an in frame deletion of a single residue at codon 173 (Q). This variant could be permanently expressed in a cytokine-dependent murine T-cell line but lacked the ability to induce proliferation in response to human IL9. In situ analyses of cells expressing the wild-type and Q receptors found both forms to be expressed at the cell surface, but the Q receptor was unable to bind hIL9 and could not be recognized by N-terminal specific antibodies. These findings demonstrate that hIL9RQ presents an altered structure and function and suggests its potential role in down-regulating IL9 signaling in effector cells and associated biological processes.

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