Immune determinants of endometrial receptivity: a biological perspective

Simple item page
dc.contributor.authorRobertson, S.A.
dc.contributor.authorMoldenhauer, L.M.
dc.contributor.authorGreen, E.S.
dc.contributor.authorCare, A.S.
dc.contributor.authorHull, M.L.
dc.date.issued2022
dc.description.abstractImmune cells are essential for endometrial receptivity to embryo implantation and early placental development. They exert tissue-remodeling and immune regulatory roles—acting to promote epithelial attachment competence, regulate the differentiation of decidual cells, remodel the uterine vasculature, control and resolve inflammatory activation, and suppress destructive immunity to paternally inherited alloantigens. From a biological perspective, the endometrial immune response exerts a form of “quality control”—it promotes implantation success when conditions are favorable but constrains receptivity when physiological circumstances are not ideal. Women with recurrent implantation failure and recurrent miscarriage may exhibit altered numbers or disturbed function of certain uterine immune cell populations—most notably uterine natural killer cells and regulatory T cells. Preclinical and animal studies indicate that deficiencies or aberrant activation states in these cells can be causal in the pathophysiological mechanisms of infertility. Immune cells are, therefore, targets for diagnostic evaluation and therapeutic intervention. However, current diagnostic tests are overly simplistic and have limited clinical utility. To be more informative, they need to account for the full complexity and reflect the range of perturbations that can occur in uterine immune cell phenotypes and networks. Moreover, safe and effective interventions to modulate these cells are in their infancy, and personalized approaches matched to specific diagnostic criteria will be needed. Here we summarize current biological understanding and identify knowledge gaps to be resolved before the promise of therapies to target the uterine immune response can be fully realized.
dc.description.statementofresponsibilitySarah A.Robertson Ph.D., Lachlan M.Moldenhauer, Ph.D, .Ella S.Green, Ph.D., Alison S.Care, Ph.D., M. Louise Hull M.B.Ch.B., Ph.D.
dc.identifier.citationFertility and Sterility, 2022; 117(6):1107-1120
dc.identifier.doi10.1016/j.fertnstert.2022.04.023
dc.identifier.issn0015-0282
dc.identifier.issn1556-5653
dc.identifier.orcidRobertson, S.A. [0000-0002-9967-0084]
dc.identifier.orcidMoldenhauer, L.M. [0000-0002-3141-2521]
dc.identifier.orcidGreen, E.S. [0000-0002-3009-3442]
dc.identifier.orcidCare, A.S. [0000-0002-0943-9453]
dc.identifier.orcidHull, M.L. [0000-0003-1813-3971] [0000-0003-4660-4005]
dc.identifier.urihttps://hdl.handle.net/2440/135417
dc.language.isoen
dc.publisherElsevier
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/APP1198172
dc.rightsCopyright © 2022 American Society for Reproductive Medicine, Published by Elsevier Inc.
dc.source.urihttps://doi.org/10.1016/j.fertnstert.2022.04.023
dc.subjectImplantation
dc.subjectimmune response
dc.subjectpregnancy tolerance
dc.subjectTreg cells
dc.subjectuNK cells
dc.subject.meshUterus
dc.subject.meshEndometrium
dc.subject.meshPlacenta
dc.subject.meshAnimals
dc.subject.meshHumans
dc.subject.meshAbortion, Habitual
dc.subject.meshEmbryo Implantation
dc.subject.meshPregnancy
dc.subject.meshFemale
dc.titleImmune determinants of endometrial receptivity: a biological perspective
dc.typeJournal article
pubs.publication-statusPublished

Files

Collections

Obstetrics and Gynaecology publications