Intravenous Infusion of Mesenchymal Stem/Stromal Cells Decreased CCR7<sup>+</sup>Antigen Presenting Cells in Mice with Corneal Allotransplantation

Lee, Hyun Ju; Ko, Jung Hwa; Ko, Ah Young; Kim, Mee Kum; Wee, Won Ryang; Oh, Joo Youn

doi:10.3109/02713683.2013.877489

Cited by 11 publications

(6 citation statements)

References 26 publications

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“… 43 Our results demonstrate that, during an immune response, MSC inhibit HEV proliferation, activation and elongation in dLNs, thus reducing the recruitment of immune cells. In agreement with our data, homing of dendritic cell to dLNs was reduced in the presence of MSC in several mouse models 44 , 45 and in vitro co-cultures of MSC with endothelial cells downregulated cytokine-induced recruitment of neutrophils and lymphocytes. 46 …”

Section: Discussionsupporting

confidence: 92%

Mouse mesenchymal stem cells inhibit high endothelial cell activation and lymphocyte homing to lymph nodes by releasing TIMP-1

et al. 2016

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Mesenchymal stem cells (MSC) represent a promising therapeutic approach in many diseases in view of their potent immunomodulatory properties, which are only partially understood. Here, we show that the endothelium is a specific and key target of MSC during immunity and inflammation. In mice, MSC inhibit activation and proliferation of endothelial cells in remote inflamed lymph nodes (LNs), affect elongation and arborization of high endothelial venules (HEVs) and inhibit T-cell homing. The proteomic analysis of the MSC secretome identified the tissue inhibitor of metalloproteinase-1 (TIMP-1) as a potential effector molecule responsible for the anti-angiogenic properties of MSC. Both in vitro and in vivo, TIMP-1 activity is responsible for the anti-angiogenic effects of MSC, and increasing TIMP-1 concentrations delivered by an Adeno Associated Virus (AAV) vector recapitulates the effects of MSC transplantation on draining LNs. Thus, this study discovers a new and highly efficient general mechanism through which MSC tune down immunity and inflammation, identifies TIMP-1 as a novel biomarker of MSC-based therapy and opens the gate to new therapeutic approaches of inflammatory diseases.

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Section: Discussionsupporting

confidence: 92%

Mouse mesenchymal stem cells inhibit high endothelial cell activation and lymphocyte homing to lymph nodes by releasing TIMP-1

et al. 2016

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“…Several studies reported MSC-derived inhibition of CD83, CD80, CD86, and HLA-DR upregulation in DC differentiation assays [ 14 , 82 – 87 ] and impairment of their migratory ability, both in vitro and in vivo , toward CCL21 [ 88 , 89 ]. In opposition, Berk et al reported that human umbilical cord blood MSC did not inhibit monocyte differentiation into immature DC and supported not only DC maturation but also the migration towards CCL21 [ 90 ].…”

Section: Discussionmentioning

confidence: 99%

Human Bone Marrow-Derived Mesenchymal Stromal Cells Differentially Inhibit Cytokine Production by Peripheral Blood Monocytes Subpopulations and Myeloid Dendritic Cells

Laranjeira¹,

Gomes

Pedreiro³

et al. 2015

Stem Cells International

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The immunosuppressive properties of mesenchymal stromal/stem cells (MSC) rendered them an attractive therapeutic approach for immune disorders and an increasing body of evidence demonstrated their clinical value. However, the influence of MSC on the function of specific immune cell populations, namely, monocyte subpopulations, is not well elucidated. Here, we investigated the influence of human bone marrow MSC on the cytokine and chemokine expression by peripheral blood classical, intermediate and nonclassical monocytes, and myeloid dendritic cells (mDC), stimulated with lipopolysaccharide plus interferon (IFN)γ. We found that MSC effectively inhibit tumor necrosis factor- (TNF-) α and macrophage inflammatory protein- (MIP-) 1β protein expression in monocytes and mDC, without suppressing CCR7 and CD83 protein expression. Interestingly, mDC exhibited the highest degree of inhibition, for both TNF-α and MIP-1β, whereas the reduction of TNF-α expression was less marked for nonclassical monocytes. Similarly, MSC decreased mRNA levels of interleukin- (IL-) 1β and IL-6 in classical monocytes, CCL3, CCL5, CXCL9, and CXCL10 in classical and nonclassical monocytes, and IL-1β and CXCL10 in mDC. MSC do not impair the expression of maturation markers in monocytes and mDC under our experimental conditions; nevertheless, they hamper the proinflammatory function of monocytes and mDC, which may impede the development of inflammatory immune responses.

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“…Unlike injured sites where tissue repair is promoted 84-87,133 and in organ transplant settings where the probability of rejection of transplant tissues is decreased 94,95,103 , the immunosuppressive action of MSCs may result in the suppression of cancer immunity in tumors, enabling cancer cells to escape immune surveillance. As observed in tissue repair processes, MSCs can influence almost all the components of the immune system to attenuate inflammation and control immune response by interfering with various immune phenomena, such as cytokine secretion and the cytotoxicity of T- and NK cells, B-cell maturation and antibody secretion, and APC maturation, activation, and function 102,134,135 .…”

Section: Mscs and Tumor Microenvironmentmentioning

confidence: 99%

Mesenchymal stromal cells’ role in tumor microenvironment: involvement of signaling pathways

Kamdje

Kamga

Tagne

et al. 2017

Cancer Biology & Medicine

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Mesenchymal stromal cells (MSCs) are adult multipotent stem cells residing as pericytes in various tissues and organs where they can differentiate into specialized cells to replace dying cells and damaged tissues. These cells are commonly found at injury sites and in tumors that are known to behave like " wounds that do not heal.” In this article, we discuss the mechanisms of MSCs in migrating, homing, and repairing injured tissues. We also review a number of reports showing that tumor microenvironment triggers plasticity mechanisms in MSCs to induce malignant neoplastic tissue formation, maintenance, and chemoresistance, as well as tumor growth. The antitumor properties and therapeutic potential of MSCs are also discussed.

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Intravenous Infusion of Mesenchymal Stem/Stromal Cells Decreased CCR7⁺Antigen Presenting Cells in Mice with Corneal Allotransplantation

Abstract: IV hMSCs reduced the activation and migration of CCR7(+) APCs in the cornea and DLNs in allogeneic corneal transplantation.

Cited by 11 publications

References 26 publications

Mouse mesenchymal stem cells inhibit high endothelial cell activation and lymphocyte homing to lymph nodes by releasing TIMP-1

Mouse mesenchymal stem cells inhibit high endothelial cell activation and lymphocyte homing to lymph nodes by releasing TIMP-1

Human Bone Marrow-Derived Mesenchymal Stromal Cells Differentially Inhibit Cytokine Production by Peripheral Blood Monocytes Subpopulations and Myeloid Dendritic Cells

Mesenchymal stromal cells’ role in tumor microenvironment: involvement of signaling pathways

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Intravenous Infusion of Mesenchymal Stem/Stromal Cells Decreased CCR7+Antigen Presenting Cells in Mice with Corneal Allotransplantation

Abstract: IV hMSCs reduced the activation and migration of CCR7(+) APCs in the cornea and DLNs in allogeneic corneal transplantation.

Cited by 11 publications

References 26 publications

Mouse mesenchymal stem cells inhibit high endothelial cell activation and lymphocyte homing to lymph nodes by releasing TIMP-1

Mouse mesenchymal stem cells inhibit high endothelial cell activation and lymphocyte homing to lymph nodes by releasing TIMP-1

Human Bone Marrow-Derived Mesenchymal Stromal Cells Differentially Inhibit Cytokine Production by Peripheral Blood Monocytes Subpopulations and Myeloid Dendritic Cells

Mesenchymal stromal cells’ role in tumor microenvironment: involvement of signaling pathways

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Intravenous Infusion of Mesenchymal Stem/Stromal Cells Decreased CCR7⁺Antigen Presenting Cells in Mice with Corneal Allotransplantation