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Clinical and Diagnostic Laboratory Immunology, September 1999, p. 660-664, Vol. 6, No. 5
1071-412X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Increased Levels of Alternatively Spliced Interleukin 4 (IL-42) Transcripts in Peripheral Blood Mononuclear Cells from Patients with Systemic Sclerosis

Lazaros I. Sakkas,¹ Charles Tourtellotte,² Steve Berney,² Allen R. Myers,² and Chris D. Platsoucas^1,*

Department of Microbiology and Immunology¹ and Section of Rheumatology, Department of Medicine,² Temple University School of Medicine, Philadelphia, Pennsylvania 19140

Received 7 January 1999/Returned for modification 17 March 1999/Accepted 2 June 1999

Recent in vitro studies have shown that interleukin 4 (IL-4) induces and gamma interferon (IFN-) inhibits collagen production. To define the TH1(IFN-) and TH2(IL-4) cytokine profiles in systemic sclerosis (Sscl), a disease characterized by widespread fibrosis, we investigated IL-4 and IFN- transcripts in peripheral blood mononuclear cells and plasma protein levels in 13 patients with Sscl. Two previously identified IL-4 transcripts, a full-length transcript and an alternatively spliced (truncated) transcript (designated IL-42), were identified in patients and normal controls. Significantly increased levels of total IL-4 transcripts (full-length plus IL-42 transcripts) were found in patients with Sscl in comparison to those found in healthy controls (P = 0.003), and this increase was primarily due to an increase in the level of the alternatively spliced IL-42 form. The IL-42/full-length-IL-4 transcript ratio was significantly increased in Sscl patients (P < 0.0001, versus healthy controls). Sequencing analysis revealed that the frequency of IL-4 clones carrying the IL-42 transcript was also substantially increased in patients with Sscl. Plasma IL-4 protein levels were increased in Sscl patients compared to those in healthy controls (P = 0.001) and correlated with total IL-4 transcript levels. The up-regulation of the fibrogenic IL-4 (a TH2 cytokine) in Sscl suggests a pathogenic role for IL-4 in this disease.

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^* Corresponding author. Mailing address: Department of Microbiology and Immunology, Temple University School of Medicine, 3400 N. Broad St., Philadelphia, PA 19140. Phone: (215) 707-7929. Fax: (215) 707-7788. E-mail: cplatsoucas{at}vm.temple.edu.

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Clinical and Diagnostic Laboratory Immunology, September 1999, p. 660-664, Vol. 6, No. 5
1071-412X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

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