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Volume 271, Number 38, Issue of September 20, 1996 pp. 23055-23060
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

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Identification and Characterization of Two Alternative Splice Variants of Human Interleukin-2

(Received for publication, May 17, 1996)

Vjacheslav N. Tsytsikov , Vladimir V. Yurovsky , Sergei P. Atamas , William J. Alms and Barbara White ^¶

From the  Division of Rheumatology & Clinical Immunology, Department of Medicine, University of Maryland at Baltimore and the ^¶ Medicine and Research Services, Veterans Affairs Medical Center, Baltimore, Maryland 21201

Our previous work showed that alternative splicing is used to make an inhibitory variant of human interleukin (IL)-4. Because of homology between IL-4 and IL-2 proteins and receptors, we tested whether alternative splicing is used to generate similar inhibitory variants of human IL-2. Messenger RNA from peripheral blood mononuclear cells was subjected to reverse transcription-polymerase chain reaction using IL-2 exon 1- and exon 4-specific primers. Two amplification products, named IL-22 and IL-23, were found in addition to the native IL-2 product. The IL-22 cDNA sequence was identical to IL-2 cDNA throughout the entire coding region, except exon 2 was omitted by alternative splicing. In IL-23 cDNA, the third exon of IL-2 was omitted by alternative splicing. Unlike IL-2, IL-22 and IL-23 did not stimulate T cell proliferation. However, both inhibited IL-2 costimulation of T cell proliferation, and both inhibited cellular binding of rhIL-2 to high affinity IL-2 receptors. Thus, IL-2 is the second cytokine that uses alternative splicing to generate variants that are competitive inhibitors.

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