Human trophoblast cell resistance to decidual NK lysis is due to lack of NK target structure

King, Ashley; Kalra, Prajakti; Loke, Y.W.

doi:10.1016/0008-8749(90)90128-e

Cited by 40 publications

(7 citation statements)

References 17 publications

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“…The majority of dNK cells are CD56 bright CD16 neg and they express a repertoire of activating and inhibitory receptors (NKRs) that resembles that of early differentiation stages of pNK cells [9], [16]–[19]. The lack of dNK cell cytotoxicity has been attributed to defects in the formation of the immunological synapse and/or failure of 2B4 receptor to convey activating signals [8], [20], [21].…”

Section: Introductionmentioning

confidence: 99%

Human Cytomegalovirus Infection Elicits New Decidual Natural Killer Cell Effector Functions

Siewiera

Costa²,

Tabiasco³

et al. 2013

PLoS Pathog

142

166

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During the first trimester of pregnancy the uterus is massively infiltrated by decidual natural killer cells (dNK). These cells are not killers, but they rather provide a microenvironment that is propitious to healthy placentation. Human cytomegalovirus (HCMV) is the most common cause of intrauterine viral infections and a known cause of severe birth defects or fetal death. The rate of HCMV congenital infection is often low in the first trimester of pregnancy. The mechanisms controlling HCMV spreading during pregnancy are not yet fully revealed, but evidence indicating that the innate immune system plays a role in controlling HCMV infection in healthy adults exists. In this study, we investigated whether dNK cells could be involved in controlling viral spreading and in protecting the fetus against congenital HCMV infection. We found that freshly isolated dNK cells acquire major functional and phenotypic changes when they are exposed to HCMV-infected decidual autologous fibroblasts. Functional studies revealed that dNK cells, which are mainly cytokines and chemokines producers during normal pregnancy, become cytotoxic effectors upon their exposure to HCMV-infected autologous decidual fibroblasts. Both the NKG2D and the CD94/NKG2C or 2E activating receptors are involved in the acquired cytotoxic function. Moreover, we demonstrate that CD56pos dNK cells are able to infiltrate HCMV-infected trophoblast organ culture ex-vivo and to co-localize with infected cells in situ in HCMV-infected placenta. Taken together, our results present the first evidence suggesting the involvement of dNK cells in controlling HCMV intrauterine infection and provide insights into the mechanisms through which these cells may operate to limit the spreading of viral infection to fetal tissues.

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Section: Introductionmentioning

confidence: 99%

Human Cytomegalovirus Infection Elicits New Decidual Natural Killer Cell Effector Functions

Siewiera

Costa²,

Tabiasco³

et al. 2013

PLoS Pathog

142

166

View full text Add to dashboard Cite

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“…Trophoblast is reported to lack recognition structures for NK cells. 28 Activatory species of Ly49 and CD94/NKG2 on NK cells (and on certain T cells) could react to typical Class I-a major histocompatibility complex (MHC) or atypical Class I-b MHC, but surface expression of such molecules on trophoblast on day 6.5 of gestation, when cellular infiltration by asialoGM1 + cells and macrophages begins, has not been shown. 29 Furthermore, as only a proportion of implant sites are infiltrated, 9 there would need to be differential expression of such determinants from implant to implant.…”

Section: Discussionmentioning

confidence: 99%

TH1/TH2,3 Imbalance due to Cytokine‐Producing NK, γδ T and NK‐γδ T Cells in Murine Pregnancy Decidua in Success or Failure of Pregnancy

Clark¹,

Croitoru²

2001

American J Rep Immunol

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gammadelta+ cells in decidua (e.g. Vgamma1+ cells which can recognize trophoblasts) differ based on the presence or absence of the NK marker-asialo-GM1. NK-gammadelta T cells may be quite important in the Th1 response in early pregnancy that predisposes to abortions in CBA x DBA/2 matings, whereas gammadelta T-only cells appear to be protective. In pregnant SCID mice, the TNF-alpha+/TGF-beta2+ NK population is greatly expanded. An activating stimulus (such as stress or endotoxin) appears to be as important in triggering abortions, as is the Th1/Th2,3 ratio at the feto maternal interface.

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“…The discovery of high numbers of large granular lymphocytes (LGL) in human decidua, later identified as decidual Natural Killer cells (dNK), led to the hypothesis that fetal placental cells actively inhibit maternal dNK and avoid immunologic rejection (King et al, 1989; King et al, 1990). The characterization of dNK as poor cytotoxic lymphocytes and major cytokine and growth factor producers distinguished dNK function from that of cytotoxic peripheral blood NK cells (pNK) (Hanna et al, 2006; Koopman et al, 2003).…”

Section: Decidual Nk Cellsmentioning

confidence: 99%

Cytotoxic potential of decidual NK cells and CD8+ T cells awakened by infections

Crespo

Zwan

Ramalho‐Santos

et al. 2017

Journal of Reproductive Immunology

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To establish a healthy pregnancy the maternal immune system must tolerate fetal allo-antigens, yet remain competent to respond to infections. The ability of decidual NK cells (dNK) to promote migration of fetal extravillous trophoblasts (EVT) and placental growth as well as the capacity of EVT to promote immune tolerance are topics of high interest and extensive research. However, the problem of how dNK and decidual CD8+ T cells (CD8+ dT) provide immunity to infections of the placenta and the mechanisms that regulate their cytolytic function has thus far largely been ignored. Fetal EVT are the most invasive cells of the placenta and directly interact with maternal decidual immune cells at this maternal-fetal interface. Besides the expression of non-polymorphic HLA-E and HLA-G molecules that are associated with immune tolerance, EVT also express highly polymorphic HLA-C molecules that can serve as targets for maternal dNK and CD8+ dT responses. HLA-C expression by EVT has a dual role as the main molecule to which immune tolerance needs to be established and as the only molecule that can present pathogen-derived peptides and provide protective immunity when EVT are infected. The focus of this review is to address the regulation of cytotoxicity of dNK and CD8+ dT, which is essential for maternal-fetal immune tolerance as well as recent evidence that both cell types can provide immunity to infections at the maternal-fetal interface. A particular emphasis is given to the role of HLA-C expressed by EVT and its capacity to elicit dNK and CD8+ dT responses.

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Human trophoblast cell resistance to decidual NK lysis is due to lack of NK target structure

Cited by 40 publications

References 17 publications

Human Cytomegalovirus Infection Elicits New Decidual Natural Killer Cell Effector Functions

Human Cytomegalovirus Infection Elicits New Decidual Natural Killer Cell Effector Functions

TH1/TH2,3 Imbalance due to Cytokine‐Producing NK, γδ T and NK‐γδ T Cells in Murine Pregnancy Decidua in Success or Failure of Pregnancy

Cytotoxic potential of decidual NK cells and CD8+ T cells awakened by infections

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