Human amniotic epithelial cells suppress relapse of corticosteroid-remitted experimental autoimmune disease

Liu, Yuhan; Chan, James; Vaghjiani, Vijesh; Murthi, Padma; Manuelpillai, Ursula; Toh, Ban‐Hock

doi:10.1016/j.jcyt.2013.10.007

Cited by 20 publications

(12 citation statements)

References 30 publications

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“…The results on transplants confirmed that hAEC are capable of a functional maturation into hepatic cells in addition to their characteristic immune-modulatory and anti-inflammatory properties (12). In fact, the same cells maintain immunosuppressive properties in animal models of autoimmune/inflammatory disease (13)(14)(15). Their safety and the absence of immune rejection were confirmed after transplantation in immune-competent mouse models as well as in human volunteers and patients (16)(17)(18).…”

mentioning

confidence: 53%

“…Most of the hAEC analyzed express intracellular IL-21, suggesting that they are able to support the in vitro survival of resting B lymphocytes as well as B cell proliferation in the presence of polyclonal stimuli. These data should be taken into account in hAEC-based treatments of autoimmune diseases related to B cell activation because preclinical experiments in animal models were successful (13)(14)(15).…”

Section: Discussionmentioning

confidence: 99%

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Ectonucleotidase Expression on Human Amnion Epithelial Cells: Adenosinergic Pathways and Dichotomic Effects on Immune Effector Cell Populations

Morandi

Horenstein

Quarona

et al. 2019

The Journal of Immunology

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This study investigates the mechanism(s) underlying the immunoregulatory activities of placenta-derived human amnion epithelial cells (hAEC). The working hypothesis is that NAD + and ATP, along with ectoenzymes involved in their metabolism, play a significant role in hAEC-mediated immune regulation. Proof of principle of the hypothesis was obtained by analyzing the interactions between hAEC and the main human leukocyte populations. The results obtained indicate that hAEC constitutively express a unique combination of functional ectoenzymes, driving the production of adenosine (ADO) via canonical (CD39, CD73) and alternative (CD38, CD203a/PC-1, CD73) pathways. Further, the picture is completed by the observation that hAEC express A1, A2a, and A2b ADO receptors as well as ADO deaminase, the enzyme involved in ADO catabolism. The contribution of the purinergic mediator to immunomodulation was confirmed by exposing in vitro different immune effector cells to the action of primary hAECs. B cells showed an enhanced proliferation and diminished spontaneous apoptosis when in contact with hAEC. T cell proliferation was partially inhibited by hAEC through ADO production, as confirmed by using specific ectoenzyme inhibitors. Further, hAEC induced an expansion of both T and B regulatory cells. Last, hAEC inhibited NK cell proliferation. However, the involvement of ADO-producing ectoenzymes is less apparent in this context. In conclusion, hAEC exert different in vitro immunoregulatory effects, per se, as a result of interactions with different populations of immune effector cells. These results support the view that hAEC are instrumental for regenerative medicine as well as in therapeutic applications for immune-related diseases.

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mentioning

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Ectonucleotidase Expression on Human Amnion Epithelial Cells: Adenosinergic Pathways and Dichotomic Effects on Immune Effector Cell Populations

Morandi

Horenstein

Quarona

et al. 2019

The Journal of Immunology

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“…The increase in relapses postpartum coincides with dramatic hormonal shifts and loss of the immunotolerant state of pregnancy [ 272 , 273 ]. A number of immune mechanisms have been postulated, including, classically, induced shifts from T-helper 1 to T-helper 2 responses [ 281 ], as well as fetal HLA-maternal killer immunoglobulin-like receptors interactions [ 282 , 283 ], microchimerism derived from fetal cells or antigens [ 284 , 285 ], and placenta-derived immunoregulation [ 286 ]. Hormonal signaling during breastfeeding, reflecting the metabolic demands placed on the mother [ 287 , 288 ], may also play a role in modulating immune activity and relapse susceptibility in MS [ 289 ].…”

Section: Theoretical Framework Initial Findings and Predictionsmentioning

confidence: 99%

Why monkeys do not get multiple sclerosis (spontaneously)

Bove

2018

Evolution, Medicine, and Public Health

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The goal of this review is to apply an evolutionary lens to understanding the origins of multiple sclerosis (MS), integrating three broad observations. First, only humans are known to develop MS spontaneously. Second, humans have evolved large brains, with characteristically large amounts of metabolically costly myelin. This myelin is generated over long periods of neurologic development—and peak MS onset coincides with the end of myelination. Third, over the past century there has been a disproportionate increase in the rate of MS in young women of childbearing age, paralleling increasing westernization and urbanization, indicating sexually specific susceptibility in response to changing exposures. From these three observations about MS, a life history approach leads us to hypothesize that MS arises in humans from disruption of the normal homeostatic mechanisms of myelin production and maintenance, during our uniquely long myelination period. This review will highlight under-explored areas of homeostasis in brain development, that are likely to shed new light on the origins of MS and to raise further questions about the interactions between our ancestral genes and modern environments.

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“…Studies on the nervous system have also reported that AECs inhibit microglia activation, reduce brain edema, and improve neurological deficit in a rat model of intracerebral hemorrhage through downregulation of TNF-α, Il-1β, and MMP-12 (Liang et al, 2014). The transplantation of AECs may even be beneficial against multiple sclerosis (Liu et al, 2012, 2014) and in immunosuppressant therapy with implication in pancreatic islet transplantation (Qureshi et al, 2011). …”

Section: Combat Inflammagingmentioning

confidence: 99%

Amniotic Epithelial Cells: A New Tool to Combat Aging and Age-Related Diseases?

Germanio

Bernier

Cabo

et al. 2016

Front. Cell Dev. Biol.

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The number of elderly people is growing at an unprecedented rate and this increase of the aging population is expected to have a direct impact on the incidence of age-related diseases and healthcare-associated costs. Thus, it is imperative that new tools are developed to fight and slow age-related diseases. Regenerative medicine is a promising strategy for the maintenance of health and function late in life; however, stem cell-based therapies face several challenges including rejection and tumor transformation. As an alternative, the placenta offers an extraordinary source of fetal stem cells, including the amniotic epithelial cells (AECs), which retain some of the characteristics of embryonic stem cells, but show low immunogenicity, together with immunomodulatory and anti-inflammatory activities. Because of these characteristics, AECs have been widely utilized in regenerative medicine. This perspective highlights different mechanisms triggered by transplanted AECs that could be potentially useful for anti-aging therapies, which include: Graft and differentiation for tissue regeneration in age-related settings, anti-inflammatory behavior to combat “inflammaging,” anti-tumor activity, direct lifespan and healthspan extension properties, and possibly rejuvenation in a manner reminiscent of heterochronic parabiosis. Here, we critically discuss benefits and limitation of AECs-based therapies in age-related diseases.

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Human amniotic epithelial cells suppress relapse of corticosteroid-remitted experimental autoimmune disease

Cited by 20 publications

References 30 publications

Ectonucleotidase Expression on Human Amnion Epithelial Cells: Adenosinergic Pathways and Dichotomic Effects on Immune Effector Cell Populations

Ectonucleotidase Expression on Human Amnion Epithelial Cells: Adenosinergic Pathways and Dichotomic Effects on Immune Effector Cell Populations

Why monkeys do not get multiple sclerosis (spontaneously)

Amniotic Epithelial Cells: A New Tool to Combat Aging and Age-Related Diseases?

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