Amnion-Derived Multipotent Progenitor Cells Inhibit Blood Monocyte Differentiation into Mature Dendritic Cells

Banas, R.; Miller, Carrie Lewis; Guzik, Lynda; Zeevi, Adriana

doi:10.3727/096368913x670165

Cited by 34 publications

(32 citation statements)

References 49 publications

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“…Furthermore, not only T lymphocytes but also the in vitro proliferation of B cells (Li et al , ), the cytotoxicity of natural killer cells (Li et al , ) and the migration of neutrophils and macrophages (Li et al , ; Tan et al , ) have been shown to be affected by amniotic cells and their CM. Moreover, we and others have demonstrated that amniotic cells and their CM impair the development of dendritic cells from primary monocytes (Magatti et al , ; Kronsteiner et al , ; Banas et al , ; Magatti et al , ). Interestingly, dendritic cell differentiation was not only blocked at the monocyte level, but skewed toward macrophage‐like cells (Magatti et al , ).…”

Section: Introductionmentioning

confidence: 74%

Human amnion favours tissue repair by inducing the M1-to-M2 switch and enhancing M2 macrophage features

Magatti

Vertua

Munari

et al. 2016

J Tissue Eng Regen Med

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Human amniotic mesenchymal cells (hAMTCs) possess interesting immunomodulatory properties, making them attractive candidates for regenerative medicine applications. Recent in vivo reports argue in favour of an important role for macrophages as targets of hAMTC‐mediated suppression of inflammation and the enhancement of tissue repair. However, a comprehensive study of the effects of hAMTCs and their conditioned medium (CM) on human macrophage differentiation and function is unavailable. In the present study we found that hAMTCs and CM induce the differentiation of myeloid cells (U937 and monocytes) towards macrophages. We then investigated their effects on monocytes differentiated toward pro‐inflammatory M1 and anti‐inflammatory M2 macrophages. Monocytes treated under M1 conditions in the presence of hAMTCs or CMs shifted towards M2‐like macrophages, which expressed CD14, CD209, CD23, CD163 and PM‐2 K, possessed higher phagocytic activity and produced higher IL‐10 and lower pro‐inflammatory cytokines. They were also poor T cell stimulators and Th1 inducers, while they were able to increase activated and naïve suppressive Treg subsets. We show that prostaglandins, and not IL‐6, play a role in determining the M2 activation status. Instead, monocytes treated under M2 conditions in the presence of hAMTCs or CM retained M2‐like features, but with an enhanced anti‐inflammatory profile, having a reduced expression of the co‐stimulatory molecule CD80, reduced phagocytosis activity and decreased the secretion of inflammatory chemokines. Importantly, we provide evidence that macrophages re‐educated by CM improve tissue regeneration/repair in wound‐healing models. In conclusion, we identified new cell targets of hAMTCs and their bioactive factors and here provide insight into the beneficial effects observed when these cells are used in therapeutic approaches in vivo. © 2016 The Authors Journal of Tissue Engineering and Regenerative Medicine Published by John Wiley & Sons Ltd.

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Section: Introductionmentioning

confidence: 74%

Human amnion favours tissue repair by inducing the M1-to-M2 switch and enhancing M2 macrophage features

Magatti

Vertua

Munari

et al. 2016

J Tissue Eng Regen Med

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“…A likely explanation of the beneficial effects exerted by hAMSC is associated to the immunomodulatory potential of these cells, a characteristic identified previously in MSC from other sources, such as bone marrow [ 37 – 40 ]. Indeed, it has been extensively reported that hAMSC can inhibit T cell proliferation induced by alloantigens, T-cell receptor cross-linking, or mitogens in vitro [ 13 – 15 , 17 , 19 ] and can inhibit the generation, maturation and function of monocyte-derived dendritic cells (DCs) [ 18 , 41 ]. The confirmation that the molecules released from cells are the key players in their immunomodulatory effect comes from the observation that the conditioned medium obtained from the culture of both AM patches and hAMSC inhibit T cell proliferation [ 27 ], inhibit the differentiation of monocytes towards DCs and induce a shift toward M2-like macrophages [ 28 , 29 ].…”

Section: Discussionmentioning

confidence: 99%

“…For example, we and others have shown that hAMSC can inhibit T cell proliferation in vitro induced by alloantigens, T-cell receptor cross-linking, or mitogens [ 13 – 17 ]. Furthermore, we and others have previously shown that cells derived from the human amniotic membrane strongly inhibit the generation, maturation, and function of monocyte-derived dendritic cells (DCs) in vitro [ 18 , 19 ]. The in-vitro anti-inflammatory potential of amniotic cells is in line with the in vivo findings showing reduction of inflammation and fibrosis in animal models of disease following the transplantation of cells derived from the amniotic membrane.…”

Section: Introductionmentioning

confidence: 99%

Amniotic Membrane Mesenchymal Cells-Derived Factors Skew T Cell Polarization Toward Treg and Downregulate Th1 and Th17 Cells Subsets

Pianta

Signoroni

Muradore

et al. 2014

Stem Cell Rev and Rep

117

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We previously demonstrated that cells derived from the mesenchymal layer of the human amniotic membrane (hAMSC) and their conditioned medium (CM-hAMSC) modulate lymphocyte proliferation in a dose-dependent manner. In order to understand the mechanisms involved in immune regulation exerted by hAMSC, we analyzed the effects of CM-hAMSC on T-cell polarization towards Th1, Th2, Th17, and T-regulatory (Treg) subsets. We show that CM-hAMSC equally suppresses the proliferation of both CD4+ T-helper (Th) and CD8+ cytotoxic T-lymphocytes. Moreover, we prove that the CM-hAMSC inhibitory ability affects both central (CD45RO+CD62L+) and effector memory (CD45RO+CD62L−) subsets. We evaluated the phenotype of CD4+ cells in the MLR setting and showed that CM-hAMSC significantly reduced the expression of markers associated to the Th1 (T-bet+CD119+) and Th17 (RORγt+CD161+) populations, while having no effect on the Th2 population (GATA3+CD193+/GATA3+CD294+cells). T-cell subset modulation was substantiated through the analysis of cytokine release for 6 days during co-culture with alloreactive T-cells, whereby we observed a decrease in specific subset-related cytokines, such as a decrease in pro-inflammatory, Th1-related (TNFα, IFNγ, IL-1β), Th2 (IL-5, IL-6), Th9 (IL-9), and Th17 (IL-17A, IL-22). Furthermore, CM-hAMSC significantly induced the Treg compartment, as shown by an induction of proliferating CD4+FoxP3+ cells, and an increase of CD25+FoxP3+ and CD39+FoxP3+ Treg in the CD4+ population. Induction of Treg cells was corroborated by the increased secretion of TGF-β. Taken together, these data strengthen the findings regarding the immunomodulatory properties of CM-hAMSC derived from human amniotic membrane MSC, and in particular provide insights into their effect on regulation of T cell polarization.

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“…14 Amniotic cells and their secreted factors possess in vitro and in vivo immune-modulatory properties. They inhibit T-cell proliferation, [15][16][17][18] reduce the production of proinflammatory cytokines, 6,7,18,19 block the differentiation/maturation of monocytes into dendritic cells, [20][21][22] promote macrophage polarization toward an M2 anti-inflammatory phenotype, 8,23,24 induce regulatory T cells, 18,25,26 and reduce natural killer cytotoxicity. 27 However, to the best of our knowledge, no studies investigated the crosstalk between hAMSCs and immune cell populations that are involved in bleomycin-induced lung injury.…”

Section: Introductionmentioning

confidence: 99%

Amniotic MSCs reduce pulmonary fibrosis by hampering lung B-cell recruitment, retention, and maturation

Cargnoni

Romele

Signoroni

et al. 2020

Stem Cells Translational Medicine

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Growing evidence suggests a mechanistic link between inflammation and the development and progression of fibrotic processes. Mesenchymal stromal cells derived from the human amniotic membrane (hAMSCs), which display marked immunomodulatory properties, have been shown to reduce bleomycin‐induced lung fibrosis in mice, possibly by creating a microenvironment able to limit the evolution of chronic inflammation to fibrosis. However, the ability of hAMSCs to modulate immune cells involved in bleomycin‐induced pulmonary inflammation has yet to be elucidated. Herein, we conducted a longitudinal study of the effects of hAMSCs on alveolar and lung immune cell populations upon bleomycin challenge. Immune cells collected through bronchoalveolar lavage were examined by flow cytometry, and lung tissues were used to study gene expression of markers associated with different immune cell types. We observed that hAMSCs increased lung expression of T regulatory cell marker Foxp3, increased macrophage polarization toward an anti‐inflammatory phenotype (M2), and reduced the antigen‐presentation potential of macrophages and dendritic cells. For the first time, we demonstrate that hAMSCs markedly reduce pulmonary B‐cell recruitment, retention, and maturation, and counteract the formation and expansion of intrapulmonary lymphoid aggregates. Thus, hAMSCs may hamper the self‐maintaining inflammatory condition promoted by B cells that continuously act as antigen presenting cells for proximal T lymphocytes in injured lungs. By modulating B‐cell response, hAMSCs may contribute to blunting of the chronicization of lung inflammatory processes with a consequent reduction of the progression of the fibrotic lesion.

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Amnion-Derived Multipotent Progenitor Cells Inhibit Blood Monocyte Differentiation into Mature Dendritic Cells

Cited by 34 publications

References 49 publications

Human amnion favours tissue repair by inducing the M1-to-M2 switch and enhancing M2 macrophage features

Human amnion favours tissue repair by inducing the M1-to-M2 switch and enhancing M2 macrophage features

Amniotic Membrane Mesenchymal Cells-Derived Factors Skew T Cell Polarization Toward Treg and Downregulate Th1 and Th17 Cells Subsets

Amniotic MSCs reduce pulmonary fibrosis by hampering lung B-cell recruitment, retention, and maturation

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