Influence of Immune System Abnormalities Caused by Maternal Immune Activation in the Postnatal Period

Cells. 2023 Feb 25;12(5):741. doi: 10.3390/cells12050741.

Abstract

The developmental origins of health and disease (DOHaD) indicate that fetal tissues and organs in critical and sensitive periods of development are susceptible to structural and functional changes due to the adverse environment in utero. Maternal immune activation (MIA) is one of the phenomena in DOHaD. Exposure to maternal immune activation is a risk factor for neurodevelopmental disorders, psychosis, cardiovascular diseases, metabolic diseases, and human immune disorders. It has been associated with increased levels of proinflammatory cytokines transferred from mother to fetus in the prenatal period. Abnormal immunity induced by MIA includes immune overreaction or immune response failure in offspring. Immune overreaction is a hypersensitivity response of the immune system to pathogens or allergic factor. Immune response failure could not properly fight off various pathogens. The clinical features in offspring depend on the gestation period, inflammatory magnitude, inflammatory type of MIA in the prenatal period, and exposure to prenatal inflammatory stimulation, which might induce epigenetic modifications in the immune system. An analysis of epigenetic modifications caused by adverse intrauterine environments might allow clinicians to predict the onset of diseases and disorders before or after birth.

Keywords: epigenetic modification; immune disorders; immune overreaction; immune response failure; maternal immune activation; maternal infection.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cytokines
  • Female
  • Humans
  • Immune System / metabolism
  • Mothers
  • Parturition
  • Pregnancy
  • Prenatal Exposure Delayed Effects*

Substances

  • Cytokines

Grants and funding

This work was supported by JSPS KAKENHI (grant numbers 15K09713, 15K15405, 16H05364, 18K11659, 19K22696, 25293241, 24659512, 22390216, and 19390291).