Pregnancy and pregnancy-associated hormones alter immune responses and disease pathogenesis

Dionne P. Robinson, Sabra L. Klein

Research output: Contribution to journalReview articlepeer-review


This article is part of a Special Issue "Neuroendocrine-Immune Axis in Health and Disease.". During pregnancy, it is evolutionarily advantageous for inflammatory immune responses that might lead to fetal rejection to be reduced and anti-inflammatory responses that promote transfer of maternal antibodies to the fetus to be increased. Hormones modulate the immunological shift that occurs during pregnancy. Estrogens, including estradiol and estriol, progesterone, and glucocorticoids increase over the course of pregnancy and affect transcriptional signaling of inflammatory immune responses at the maternal-fetal interface and systemically. During pregnancy, the reduced activity of natural killer cells, inflammatory macrophages, and helper T cell type 1 (Th1) cells and production of inflammatory cytokines, combined with the higher activity of regulatory T cells and production of anti-inflammatory cytokines, affects disease pathogenesis. The severity of diseases caused by inflammatory responses (e.g., multiple sclerosis) is reduced and the severity of diseases that are mitigated by inflammatory responses (e.g., influenza and malaria) is increased during pregnancy. For some infectious diseases, elevated inflammatory responses that are necessary to control and clear a pathogen have a negative consequence on the outcome of pregnancy. The bidirectional interactions between hormones and the immune system contribute to both the outcome of pregnancy and female susceptibility to disease.

Original languageEnglish (US)
Pages (from-to)263-271
Number of pages9
JournalHormones and Behavior
Issue number3
StatePublished - Aug 2012


  • Autoimmunity
  • Estrogen
  • IFN-γ
  • IL-10
  • Influenza
  • Malaria
  • Multiple sclerosis
  • Progesterone
  • Regulatory T cell
  • Th1/Th2

ASJC Scopus subject areas

  • Endocrinology
  • Endocrine and Autonomic Systems
  • Behavioral Neuroscience


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