Pathogenesis of preterm birth: bidirectional inflammation in mother and fetus

Ella Shana Green; Petra Clara Arck

doi:10.1007/s00281-020-00807-y

Pathogenesis of preterm birth: bidirectional inflammation in mother and fetus

Standard

Pathogenesis of preterm birth: bidirectional inflammation in mother and fetus. / Green, Ella Shana; Arck, Petra Clara.

In: SEMIN IMMUNOPATHOL, Vol. 42, No. 4, 30.08.2020, p. 413-429.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Green, ES & Arck, PC 2020, 'Pathogenesis of preterm birth: bidirectional inflammation in mother and fetus', SEMIN IMMUNOPATHOL, vol. 42, no. 4, pp. 413-429. https://doi.org/10.1007/s00281-020-00807-y

APA

Green, E. S., & Arck, P. C. (2020). Pathogenesis of preterm birth: bidirectional inflammation in mother and fetus. SEMIN IMMUNOPATHOL, 42(4), 413-429. https://doi.org/10.1007/s00281-020-00807-y

Vancouver

Green ES, Arck PC. Pathogenesis of preterm birth: bidirectional inflammation in mother and fetus. SEMIN IMMUNOPATHOL. 2020 Aug 30;42(4):413-429. https://doi.org/10.1007/s00281-020-00807-y

Bibtex

@article{6cc6f6ad15494429bdd224d7da210eb0,

title = "Pathogenesis of preterm birth: bidirectional inflammation in mother and fetus",

abstract = "Preterm birth (PTB) complicates 5-18% of pregnancies globally and is a leading cause of maternal and fetal morbidity and mortality. Most PTB is spontaneous and idiopathic, with largely undefined causes. To increase understanding of PTB, much research in recent years has focused on using animal models to recapitulate the pathophysiology of PTB. Dysfunctions of maternal immune adaptations have been implicated in a range of pregnancy pathologies, including PTB. A wealth of evidence arising from mouse models as well as human studies is now available to support that PTB results from a breakdown in fetal-maternal tolerance, along with excessive, premature inflammation. In this review, we examine the current knowledge of the bidirectional communication between fetal and maternal systems and its role in the immunopathogenesis of PTB. These recent insights significantly advance our understanding of the pathogenesis of PTB, which is essential to ultimately designing more effective strategies for early prediction and subsequent prevention of PTB.",

author = "Green, {Ella Shana} and Arck, {Petra Clara}",

year = "2020",

month = aug,

day = "30",

doi = "10.1007/s00281-020-00807-y",

language = "English",

volume = "42",

pages = "413--429",

journal = "SEMIN IMMUNOPATHOL",

issn = "1863-2297",

publisher = "Springer",

number = "4",

}

RIS

TY - JOUR

T1 - Pathogenesis of preterm birth: bidirectional inflammation in mother and fetus

AU - Green, Ella Shana

AU - Arck, Petra Clara

PY - 2020/8/30

Y1 - 2020/8/30

N2 - Preterm birth (PTB) complicates 5-18% of pregnancies globally and is a leading cause of maternal and fetal morbidity and mortality. Most PTB is spontaneous and idiopathic, with largely undefined causes. To increase understanding of PTB, much research in recent years has focused on using animal models to recapitulate the pathophysiology of PTB. Dysfunctions of maternal immune adaptations have been implicated in a range of pregnancy pathologies, including PTB. A wealth of evidence arising from mouse models as well as human studies is now available to support that PTB results from a breakdown in fetal-maternal tolerance, along with excessive, premature inflammation. In this review, we examine the current knowledge of the bidirectional communication between fetal and maternal systems and its role in the immunopathogenesis of PTB. These recent insights significantly advance our understanding of the pathogenesis of PTB, which is essential to ultimately designing more effective strategies for early prediction and subsequent prevention of PTB.

AB - Preterm birth (PTB) complicates 5-18% of pregnancies globally and is a leading cause of maternal and fetal morbidity and mortality. Most PTB is spontaneous and idiopathic, with largely undefined causes. To increase understanding of PTB, much research in recent years has focused on using animal models to recapitulate the pathophysiology of PTB. Dysfunctions of maternal immune adaptations have been implicated in a range of pregnancy pathologies, including PTB. A wealth of evidence arising from mouse models as well as human studies is now available to support that PTB results from a breakdown in fetal-maternal tolerance, along with excessive, premature inflammation. In this review, we examine the current knowledge of the bidirectional communication between fetal and maternal systems and its role in the immunopathogenesis of PTB. These recent insights significantly advance our understanding of the pathogenesis of PTB, which is essential to ultimately designing more effective strategies for early prediction and subsequent prevention of PTB.

U2 - 10.1007/s00281-020-00807-y

DO - 10.1007/s00281-020-00807-y

M3 - SCORING: Review article

C2 - 32894326

VL - 42

SP - 413

EP - 429

JO - SEMIN IMMUNOPATHOL

JF - SEMIN IMMUNOPATHOL

SN - 1863-2297

IS - 4

ER -