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Immunological Modes of Pregnancy Loss: Inflammation, Immune Effectors, and Stress

Authors

  • Joanne Kwak-Kim,

    Corresponding author
    1. Reproductive Medicine, Department of Obstetrics and Gynecology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, Vernon Hills, IL, USA
    2. Department of Microbiology and Immunology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA
    • Correspondence

      Joanne Kwak-Kim, Department of Obstetrics and Gynecology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, 830 West End Court, Suite 400, Vernon Hills, IL 60061, USA.

      and

      Department of Microbiology and Immunology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064, USA.

      E-mail: joanne.kwakkim@rosalindfranklin.edu

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  • Shihua Bao,

    1. Reproductive Medicine, Department of Obstetrics and Gynecology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, Vernon Hills, IL, USA
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  • Sung Ki Lee,

    1. Department of Obstetrics and Gynecology, College of Medicine, Konyang University, Seo-gu, Daejeon, Korea
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  • Joon Woo Kim,

    1. The Division of Rheumatology, Department of Internal Medicine, Northwestern University Feinberg School of Medicine, McGaw Pavilion, Chicago, IL, USA
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  • Alice Gilman-Sachs

    1. Department of Microbiology and Immunology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA
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Abstract

Inflammatory immune response plays a key role in reproductive failures such as multiple implantation failures (MIF), early pregnancy loss, and recurrent pregnancy losses (RPL). Cellular immune responses particularly mediated by natural killer (NK), and T cells are often dysregulated in these conditions. Excessive or inappropriate recruitment of peripheral blood NK cells to the uterus may lead to cytotoxic environment in utero, in which proliferation and differentiation of trophoblast is hampered. In addition, inadequate angiogenesis by uterine NK cells often leads to abnormal vascular development and blood flow patterns, which, in turn, leads to increased oxidative stress or ischemic changes in the invading trophoblast. T-cell abnormalities with increased Th1 and Th17 immunity, and decreased Th2 and T regulatory immune responses may play important roles in RPL and MIF. A possible role of stress in inflammatory immune response is also reviewed.

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