Roles of human trophoblasts' pattern recognition receptors in host defense and pregnancy complications.
J Reprod Immunol
; 156: 103811, 2023 03.
Article
em En
| MEDLINE
| ID: mdl-36669386
The immune system in pregnancy is able to protect pregnant mothers and fetuses from pathogenic microorganisms even while permitting the mother to tolerate the semi-allogenic fetus. Trophoblasts, which are fetal-derived placental cells, play a central role on both sides of this duality at the maternal-fetal interface. In brief, the trophoblasts express pattern recognition receptors (PRRs) and are involved in the local innate immune response in the placenta. That response eliminates pathogenic microbes but also causes tissue damage. In this review, we summarize the research findings to date regarding the roles of those human trophoblast PRRs. Multiple types of PRRs (Toll-like receptors, Nod-like receptors, and RIG-I-like receptors) are expressed in the placenta and on trophoblasts. Trophoblasts' PRRs participate in protecting the fetus against viruses, bacteria, and parasites by triggering production of proinflammatory cytokines and chemokines in the placenta. On the negative side, PRR signaling in trophoblasts can also initiate inflammation and trophoblast cell death, which can lead to placental inflammation-associated pregnancy complications such as preeclampsia, anti-phospholipid antibody syndrome, and miscarriage. Further elucidation of these dual roles of trophoblasts' PRRs may shed light on the mechanisms by which fetuses are protected against congenital infections and also give us a better understanding of the etiologies of pregnancy complications, which can help us prevent/reduce adverse prenatal/neonatal outcomes.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Contexto em Saúde:
2_ODS3
/
7_ODS3_muertes_prevenibles_nacidos_ninos
Base de dados:
MEDLINE
Assunto principal:
Complicações Infecciosas na Gravidez
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Trofoblastos
Limite:
Female
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Humans
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Newborn
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Pregnancy
Idioma:
En
Revista:
J Reprod Immunol
Ano de publicação:
2023
Tipo de documento:
Article