Journal of reproductive immunology
-
J. Reprod. Immunol. · Sep 2020
ReviewCOVID-19 and immunomodulation treatment for women with reproductive failures.
COVID-19 pandemic is affecting various areas of health care, including human reproduction. Many women with reproductive failures, during the peri-implantation period and pregnancy, are on the immunotherapy using immune modulators and immunosuppressant due to underlying autoimmune diseases, cellular immune dysfunction, and rheumatic conditions. ⋯ SARS-CoV-2 is a novel virus, and not enough information exists. Yet, we aim to review the data from previous coronavirus outbreaks and current COVID-19 and provide interim guidelines for immunotherapy in women with reproductive failures.
-
J. Reprod. Immunol. · Jun 2020
ReviewWhy are pregnant women susceptible to COVID-19? An immunological viewpoint.
The 2019 novel coronavirus disease (COVID-19) was first detected in December 2019 and became epidemic in Wuhan, Hubei Province, China. COVID-19 has been rapidly spreading out in China and all over the world. The virus causing COVID-19, SARS-CoV-2 has been known to be genetically similar to severe acute respiratory syndrome coronavirus (SARS-CoV) but distinct from it. ⋯ In pregnant women with COVID-19, there is no evidence for vertical transmission of the virus, but an increased prevalence of preterm deliveries has been noticed. The COVID-19 may alter immune responses at the maternal-fetal interface, and affect the well-being of mothers and infants. In this review, we focused on the reason why pregnant women are more susceptible to COVID-19 and the potential maternal and fetal complications from an immunological viewpoint.
-
J. Reprod. Immunol. · Aug 2003
ReviewTrophoblast deportation and the maternal inflammatory response in pre-eclampsia.
We have proposed that the maternal syndrome of pre-eclampsia is caused by a systemic inflammatory response involving both leucocytes and endothelium. This inflammatory response is present also in normal pregnancy, but in a milder form. ⋯ Syncytiotrophoblast apoptotic debris, which is shed into the maternal circulation in normal pregnancy and in increased amounts in pre-eclampsia, may be the stimulus for this response. It may also contribute to the suppression of Th1 responses seen in pregnancy.