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Th1 and Th2 Cytokine Profiles in Successful Pregnancy and Unexplained Recurrent Abortions

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Reproductive Immunology

Abstract

Several studies on animal models of pregnancy and a few on human pregnancy have led to the proposition that successful pregnancy is a T helper 2 (Th2) phenomenon, while vigorous Thl-type immunity, mediated by Thl-type cytokines, is deleterious to pregnancy. With the objective of examining Th1- and Th2-type bias in normal pregnancy and in pregnancy failure, we analysed the patterns of Th1- and Th2- type cytokine production in women with a history of successful pregnancy and in women with a history of unexplained recurrent spontaneous abortions (RSA). Peripheral blood mononuclear cells (PBMC) from 54 women with a history of normal pregnancy and 23 women with a history of unexplained RSA, obtained at delivery or on the day of abortion respectively, were activated with the mitogen phytohemagglutinin (PHA), after which the levels of four Th2 cytokines and three Th 1 cytokines were estimated. We found that the PBMC of women in the normal pregnancy group produced significantly higher levels of the Th2 cytokines interleukin (IL)-4, IL-5, IL-6 and IL-10 than did the PBMC of the RSA group. On the other hand, PBMC of the women with a history of RSA secreted higher levels of the Th1-type cytokines IL-2 and tumour necrosis factor (TNF) than the normal pregnancy group. These data support the notion that Th2-dominance is a feature of successful pregnancy and that unexplained recurrent spontaneous abortion is associated with an increase in Th-1 type reactivity.

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Raghupathy, R., Makhseed, M., Azizieh, F., Al-Azemi, M.M.K., Hassan, N.A., Bandar, A. (1999). Th1 and Th2 Cytokine Profiles in Successful Pregnancy and Unexplained Recurrent Abortions. In: Gupta, S.K. (eds) Reproductive Immunology. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-4197-0_14

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  • DOI: https://doi.org/10.1007/978-94-011-4197-0_14

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-5825-4

  • Online ISBN: 978-94-011-4197-0

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