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Research Article Free access | 10.1172/JCI114023

Increased polyamines may downregulate interleukin 2 production in rheumatoid arthritis.

E Flescher, T L Bowlin, A Ballester, R Houk, and N Talal

Clinical Immunology Section, Audie L. Murphy Memorial Veterans Hospital, San Antonio, Texas.

Find articles by Flescher, E. in: PubMed | Google Scholar

Clinical Immunology Section, Audie L. Murphy Memorial Veterans Hospital, San Antonio, Texas.

Find articles by Bowlin, T. in: PubMed | Google Scholar

Clinical Immunology Section, Audie L. Murphy Memorial Veterans Hospital, San Antonio, Texas.

Find articles by Ballester, A. in: PubMed | Google Scholar

Clinical Immunology Section, Audie L. Murphy Memorial Veterans Hospital, San Antonio, Texas.

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Clinical Immunology Section, Audie L. Murphy Memorial Veterans Hospital, San Antonio, Texas.

Find articles by Talal, N. in: PubMed | Google Scholar

Published April 1, 1989 - More info

Published in Volume 83, Issue 4 on April 1, 1989
J Clin Invest. 1989;83(4):1356–1362. https://doi.org/10.1172/JCI114023.
© 1989 The American Society for Clinical Investigation
Published April 1, 1989 - Version history
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Abstract

Polyamines downregulate immune reactivity. RA is associated with decreased IL 2 production. In this study, we present evidence to suggest that excessive polyamines can contribute to the IL 2 deficiency in RA. Blocking polyamine production with inhibitors of ornithine decarboxylase results in increased IL 2 production by RA PBMC. Moreover, polyamine oxidase (PAO) inhibitors and catalase also increase IL 2 production by RA PBMC. This effect of PAO inhibition is monocyte mediated. After 3 d in culture, RA PBMC produce three times more IL 2 than do normal PBMC. This rise is prevented by exogenous spermidine but only in the presence of monocytes. The concentration of polyamines in RA PBMC and synovial fluid MNC is 2-20-fold higher than in normal cells. Thus, polyamines and their oxidation products downregulate IL 2 production by RA PBMC and may account for the decreased T cell effector function seen in this disease.

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