Trophoblast‐derived CXCL12 promotes CD56brightCD82−CD29+ NK cell enrichment in the decidua

Han, Lu; Jin, Liping; Huang, Hong-Lan; Ha, Si‐Yao; Yang, Hui‐Li; Chang, Ruiqi; Li, Da‐Jin; Li, Ming‐Qing

doi:10.1111/aji.13203

Cited by 20 publications

(8 citation statements)

References 69 publications

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“…Our previous studies have elucidated that CD82 in decidua plays many biological functions. For example, CD82 in DSCs is involved in controlling invasiveness of extravillous trophoblast (Li et al 2010), and CD82 in NK cells participates in the regulation of cell adhesion and residence in decidua during early pregnancy (Lu et al 2020). Based on this study and previous reports, we conclude that a higher level of CD82 under a positive regulation of COX-2/PGE2 promotes decidualization in vitro.…”

Section: High Intracellular Camp and Pge2 Concentrationssupporting

confidence: 74%

“…It acts as a key regulator in limiting the inappropriate invasion of trophoblasts during decidualization (Li et al 2010, Gellersen et al 2013 and inhibiting tumor cell migration and metastasis (Liu et al 2021, Ma et al 2021. Additionally, CD82 is involved in the regulation of infiltration and adhesion of decidual NK cells during early pregnancy (Lu et al 2020). However, little is known about the specific mechanism of the upregulation of CD82 in decidua and its effect on decidualization.…”

Section: Introductionmentioning

confidence: 99%

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A positive COX-2/IL-1β loop promotes decidualization by upregulating CD82

Shen

Wang

et al. 2021

Reproduction

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A successful pregnancy requires sufficient decidualization of endometrial stromal cells (ESCs). CD82, a metastasis suppressor, is a critical regulator for trophoblast invasion but the effect in decidualization was largely unknown. Here we reported that there was a high level of CD82 in DSC by the immunohistochemistry staining and flow cytometer analysis. Stimulation with prostaglandin E2 (PGE2) elevated the expression of CD82 in ESCs. In contrast, celecoxib, a selective COX-2 inhibitor, significantly down-regulated the expression of CD82 in decidual stromal cells (DSCs). Bioinformatics analysis and further research showed that recombinant human interleukin (IL)-1β protein (rhIL-1β) up-regulated CD82 in ESCs. Of note, blocking IL-1β signaling with anti-human IL-1β neutralizing antibody could reverse the stimulatory effect of PGE2 on CD82 in ESCs. Silencing CD82 resulted in the decease of the decidualization markers PRL and IGFBP1 mRNA levels in DSCs. More importantly, we observed rhIL-1β also up-regulated the expression of COX-2, and the up-regulation of PRL and IGFBP1 induced by rhIL-1β could be abolished by celecoxib in ESCs or CD82 deficiency in DSCs. This study suggests that CD82 should be a novel promotor for decidualization under a positive regulation of the COX-2/PGE2/IL-1β positive feedback loop.

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Section: High Intracellular Camp and Pge2 Concentrationssupporting

confidence: 74%

Section: Introductionmentioning

confidence: 99%

A positive COX-2/IL-1β loop promotes decidualization by upregulating CD82

Shen

Wang

et al. 2021

Reproduction

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“…Here we observed that the autophagy level of pNK cells was much lower than that of dNK, it is noteworthy that autophagy does not seem to be directly involved in the regulation of NK cell adhesion and cytotoxic activity. Along with blastocyst implantation, it is widely recognized that embryonic trophoblast cells secrete large amounts of CXCL12 at the maternal-fetal interface, which recruit and promotes the adhesion ability of NCAM1 brigh NK cells to DSCs in a CD82/ITGB1-dependetnt manner [37,38]. In this study, we found that decidualization was accompanied with the increase of autophagy, which might be due to the positive role of a significant increase in progesterone during early pregnancy [34].…”

Section: Discussionmentioning

confidence: 50%

Rapamycin prevents spontaneous abortion by triggering decidual stromal cell autophagy-mediated NK cell residence

et al. 2020

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Deficiency in decidualization has been widely regarded as an important cause of spontaneous abortion. Generalized decidualization also includes massive infiltration and enrichment of NK cells. However, the underlying mechanism of decidual NK (dNK) cell residence remains largely unknown. Here, we observe that the increased macroautophagy/autophagy of decidual stromal cells (DSCs) during decidualization, facilitates the adhesion and retention of dNK cells during normal pregnancy. Mechanistically, this process is mediated through activation of the MITF-TNFRSF14/HVEM signaling, and further upregulation of multiple adhesion adhesions (e.g. Selectins and ICAMs) in a MMP9-dependent manner. Patients with unexplained spontaneous abortion display insufficient DSC autophagy and dNK cell residence. In addition, poor vascular remodeling of placenta, low implantation number and high ratio of embryo loss are observed in NK cell depletion mice. In therapeutic studies, low doses of rapamycin, a known autophagy inducer that significantly promotes endometrium autophagy and NK cell residence, and improves embryo absorption in spontaneous abortion mice models, which should be dependent on the activation of MITF-TNFRSF14/HVEM-MMP9-adhension molecules axis. This observation reveals novel molecular mechanisms underlying DSCs autophagy-driven dNK cell residence, and provides a potential therapeutic strategy to prevent spontaneous abortion.

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“…CD56-bright NK cells only, and not the CD56dim subset, display CD117 (c-Kit) expression, high affinity receptor for IL-2 and CCR7 on their surface and express a higher level of CXCR3 (173). The CD56 bright NK cells are more potent producers of the following cytokines: IFN gamma, TNF alpha, GM-CSF, IL10, IL13.…”

Section: The Essential Role Of Cd56 In Development Of Cns Leukemiamentioning

confidence: 99%

A narrative review of central nervous system involvement in acute leukemias

Deak¹,

Gorcea-Andronic²,

Sas³

et al. 2021

Ann Transl Med

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Acute leukemias (both myeloid and lymphoblastic) are a group of diseases for which each year more successful therapies are implemented. However, in a subset of cases the overall survival (OS) is still exceptionally low due to the infiltration of leukemic cells in the central nervous system (CNS) and the subsequent formation of brain tumors. The CNS involvement is more common in acute lymphocytic leukemia (ALL), than in adult acute myeloid leukemia (AML), although the rates for the second case might be underestimated. The main reasons for CNS invasion are related to the expression of specific adhesion molecules (VLA-4, ICAM-1, VCAM, L-selectin, PECAM-1, CD18, LFA-1, CD58, CD44, CXCL12) by a subpopulation of leukemic cells, called "sticky cells" which have the ability to interact and adhere to endothelial cells. Moreover, the microenvironment becomes hypoxic and together with secretion of VEGF-A by ALL or AML cells the permeability of vasculature in the bone marrow increases, coupled with the disruption of blood brain barrier. There is a single subpopulation of leukemia cells, called leukemia stem cells (LSCs) that is able to resist in the new microenvironment due to its high adaptability. The LCSs enter into the arachnoid, migrate, and intensively proliferate in cerebrospinal fluid (CSF) and consequently infiltrate perivascular spaces and brain parenchyma. Moreover, the CNS is an immune privileged site that also protects leukemic cells from chemotherapy. CD56/NCAM is the most important surface molecule often overexpressed by leukemic stem cells that offers them the ability to infiltrate in the CNS. Although

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Trophoblast‐derived CXCL12 promotes CD56^brightCD82⁻CD29⁺ NK cell enrichment in the decidua

Cited by 20 publications

References 69 publications

A positive COX-2/IL-1β loop promotes decidualization by upregulating CD82

A positive COX-2/IL-1β loop promotes decidualization by upregulating CD82

Rapamycin prevents spontaneous abortion by triggering decidual stromal cell autophagy-mediated NK cell residence

A narrative review of central nervous system involvement in acute leukemias

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