Mesenchymal stem cells and natural killer cells interaction mechanisms and potential clinical applications

Abbasi, Batol; Shamsasenjan, Karim; Ahmadi, Majid; Beheshti, Seyedeh Ameneh; Saleh, Mahshid

doi:10.1186/s13287-022-02777-4

Cited by 28 publications

(16 citation statements)

References 173 publications

(271 reference statements)

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“…At lower doses, MSCs promoted NK cell formation and enhanced their antitumour activity against cancer cells, while at higher doses, MSCs inhibited NK cell formation and attenuated their tumour-killing effects [ 145 ]. A reasonable explanation for this dual immunomodulatory effect of MSCs on NK cells is that experimental conditions, including the MSC:NK cell ratio, cell concentration, quality of prestimulated NK cells, and coculture incubation time, affect the direction of interaction between MSCs and NK cells [ 138 , 146 ]. It has also been suggested that MSCs are inherently heterogeneous and simultaneously release proinflammatory cytokines and immune cell suppressive factors [ 147 ].…”

Section: Crosstalk Between Nk Cells and The Tmementioning

confidence: 99%

NK cells are never alone: crosstalk and communication in tumour microenvironments

Zhou

Lu²,

Liu

et al. 2023

Mol Cancer

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Immune escape is a hallmark of cancer. The dynamic and heterogeneous tumour microenvironment (TME) causes insufficient infiltration and poor efficacy of natural killer (NK) cell-based immunotherapy, which becomes a key factor triggering tumour progression. Understanding the crosstalk between NK cells and the TME provides new insights for optimising NK cell-based immunotherapy. Here, we present new advances in direct or indirect crosstalk between NK cells and 9 specialised TMEs, including immune, metabolic, innervated niche, mechanical, and microbial microenvironments, summarise TME-mediated mechanisms of NK cell function inhibition, and highlight potential targeted therapies for NK-TME crosstalk. Importantly, we discuss novel strategies to overcome the inhibitory TME and provide an attractive outlook for the future.

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Section: Crosstalk Between Nk Cells and The Tmementioning

confidence: 99%

NK cells are never alone: crosstalk and communication in tumour microenvironments

Zhou

Lu²,

Liu

et al. 2023

Mol Cancer

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“…Granzyme B, a serine protease found in the lytic granules of NK cells, orchestrates cell apoptosis, especially through Bid (i.e., a Bcl-2 family member) ( 107 ). Interestingly, elevated levels of granzyme B have been shown to increase mesenchymal stem cell (MSC) populations ( 108 ). Conversely, MSCs suppress the activity of NK and other immune cells for example by increasing tryptophan metabolites ( 109 , 110 ).…”

Section: Secondary Effector Cells – From Natural Killer Cells To Mast...mentioning

confidence: 99%

Cellular activation pathways and interaction networks in vascularized composite allotransplantation

Knoedler

Lee

et al. 2023

Front. Immunol.

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Vascularized composite allotransplantation (VCA) is an evolving field of reconstructive surgery that has revolutionized the treatment of patients with devastating injuries, including those with limb losses or facial disfigurement. The transplanted units are typically comprised of different tissue types, including skin, mucosa, blood and lymphatic vasculature, muscle, and bone. It is widely accepted that the antigenicity of some VCA components, such as skin, is particularly potent in eliciting a strong recipient rejection response following transplantation. The fine line between tolerance and rejection of the graft is orchestrated by different cell types, including both donor and recipient-derived lymphocytes, macrophages, and other immune and donor-derived tissue cells (e.g., endothelium). Here, we delineate the role of different cell and tissue types during VCA rejection. Rejection of VCA grafts and the necessity of life-long multidrug immunosuppression remains one of the major challenges in this field. This review sheds light on recent developments in decoding the cellular signature of graft rejection in VCA and how these may, ultimately, influence the clinical management of VCA patients by way of novel therapies that target specific cellular processes.

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“…In fact, the adhesion of MM cells to BM‐MSC upregulates cytokine secretion from both cell types, which in turn leads to the activation of major signalling pathways such as MEK‐ERK, JAK2/STAT3, PI3K and NF‐κβ. Downstream signalling targets include interleukin (IL)‐6, a well‐known potent driver of MM progression, as well as the immunosuppressive cytokines IL‐10 and transforming growth factor (TGF)‐β 8 …”

Section: Figurementioning

confidence: 99%

“…Downstream signalling targets include interleukin (IL)-6, a well-known potent driver of MM progression, as well as the immunosuppressive cytokines IL-10 and transforming growth factor (TGF)-β. 8 Interestingly, MM BM-MSC seems to play a more important role in NK cell exhaustion in the BM microenvironment than the malignant cells themselves. Several investigations have reported that IFN-γ secreted from activated NK cells induces the release of immunomodulatory factors (IDO1, TGF-β, HLA-G and PGE2) from BM-MSC, which in turn alter the expression of activation markers and ERK1/2 signalling in NK cells, hence modulating their cytotoxic activity.…”

mentioning

confidence: 99%

Natural killer cells and bone marrow mesenchymal stem cells: A dangerous liaison in multiple myeloma

Botana

Moussay

Paggetti

2022

Clinical and Translational Dis

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BM-MSC, immune checkpoint blockade, NK cells, TIGITAccounting for 10% of all blood cancers, multiple myeloma (MM) is an incurable haematological malignancy characterized by the accumulation of clonal plasma cells in the bone marrow (BM) of patients. This malignancy often develops in elderly patients through the accumulation of a heterogeneous range of cytogenetic abnormalities that promote tumour growth and survival in the BM microenvironment. 1 The gold standard for the treatment of newly diagnosed patients without co-morbidities remains high-dose chemotherapy plus autologous stem cell transplantation. Unfortunately, MM patients relapse after each treatment regimen, leading to a continuous and dynamic search for new non-refractory therapeutic options. 2 Novel agents including immunomodulatory drugs, proteasome inhibitors, dexamethasone and more recently monoclonal antibodies have transformed the treatment paradigm of MM. Nowadays, these agents are extensively used in the clinic to target relapsed and refractory diseases. Of particular interest, immune checkpoint inhibitors have emerged as powerful tools to disrupt the deeply immunosuppressive interactions in the BM MM microenvironment,This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Mesenchymal stem cells and natural killer cells interaction mechanisms and potential clinical applications

Cited by 28 publications

References 173 publications

NK cells are never alone: crosstalk and communication in tumour microenvironments

NK cells are never alone: crosstalk and communication in tumour microenvironments

Cellular activation pathways and interaction networks in vascularized composite allotransplantation

Natural killer cells and bone marrow mesenchymal stem cells: A dangerous liaison in multiple myeloma

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