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Clinical and Developmental Immunology
Volume 2012, Article ID 734865, 10 pages
Clinical Study

Intrauterine Growth Restriction: Cytokine Profiles of Trophoblast Antigen-Stimulated Maternal Lymphocytes

1Department of Microbiology, Faculty of Medicine, Kuwait University, P.O. Box 24923, Kuwait 13110, Kuwait
2Department of Obstetrics & Gynecology, Faculty of Medicine, Kuwait University, P.O. Box 24923, Kuwait 13110, Kuwait
3Department of Mathematics & Biology, Gulf University for Science and Technology, Mubarak Al-Abdullah Area, West Mishref, Hawalli 32093, Kuwait

Received 28 June 2011; Revised 16 August 2011; Accepted 16 August 2011

Academic Editor: Andres Salumets

Copyright © 2012 Raj Raghupathy et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Intrauterine growth restriction (IUGR) is an important perinatal syndrome that poses several serious short- and long-term effects. We studied cytokine production by maternal peripheral blood lymphocytes stimulated by trophoblast antigens. 36 women with a diagnosis of IUGR and 22 healthy women with normal fetal growth were inducted. Peripheral blood mononuclear cells were stimulated with trophoblast antigens and levels of the proinflammatory cytokines IL-6, IL-8, IL-12, IL-23, IFNγ, and TNFα and the anti-inflammatory cytokines IL-4, IL-10, and IL-13 were measured in culture supernatants by ELISA. IL-8 was produced at higher levels by blood cells of the IUGR group than normal pregnant women, while IL-13 was produced at lower levels. IL-8, IFNγ, and TNFα were higher in IUGR with placental insufficiency than in normal pregnancy. IL-12 levels were higher and IL-10 levels were lower in IUGR with placental insufficiency than in IUGR without placental insufficiency. We suggest that a stronger pro-inflammatory bias exists in IUGR as compared to normal pregnancy and in IUGR with placental insufficiency when compared to IUGR without placental insufficiency. Several ratios of proinflammatory to anti-inflammatory cytokines also support the existence of an inflammatory bias in IUGR.