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The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 12 4781-4788
Copyright © 2000 by The Endocrine Society

Original Studies

The Transforming Growth Factor-ß Superfamily Cytokine Macrophage Inhibitory Cytokine-1 Is Present in High Concentrations in the Serum of Pregnant Women1

A. G. Moore2, D. A. Brown2, W. D. Fairlie, A. R. Bauskin, P. K. Brown, M. L. C. Munier, P. K. Russell, L. A. Salamonsen, E. M. Wallace and S. N. Breit

Centre for Immunology (A.G.M., D.A.B., W.D.F., A.R.B., P.K.B., M.L.C.M., P.K.R., S.N.B.), St. Vincent’s Hospital and University of New South Wales, Sydney, New South Wales, Australia; Department of Obstetrics and Gynecology (E.M.W.), Monash University, Clayton, Victoria, Australia; and Prince Henry’s Institute of Medical Research (L.A.S.), Clayton, Victoria, Australia

Address all correspondence and requests for reprints to: Dr. Samuel N. Breit, Centre for Immunology, St. Vincent’s Hospital, Victoria Street, Sydney, New South Wales 2010, Australia. E-mail: s.breit{at}cfi.unsw.edu.au

Macrophage inhibitory cytokine-1 (MIC-1) is a recently described divergent member of the transforming growth factor-ß superfamily. MIC-1 transcription up-regulation is associated with macrophage activation, and this observation led to its cloning. Northern blots indicate that MIC-1 is also present in human placenta. A sensitive sandwich enzyme-linked immunosorbent assay for the quantification of MIC-1 was developed and used to examine the role of this cytokine in pregnancy. High levels of MIC-1 are present in the sera of pregnant women. The level rises substantially with progress of gestation. MIC-1 can also be detected, in large amounts, in amniotic fluid and placental extracts. In addition, the BeWo placental trophoblastic cell line was found to constitutively express the MIC-1 transcript and secrete large amounts of MIC-1. These findings suggest that the placental trophoblast is a major source of the MIC-1 present in maternal serum and amniotic fluid. We suggest that MIC-1 may promote fetal survival by suppressing the production of maternally derived proinflammatory cytokines within the uterus.




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