Mesenchymal stem cells alleviate rat diabetic nephropathy by suppressing CD103<sup>+</sup> DCs‐mediated CD8<sup>+</sup> T cell responses

Zhang, Fuping; Wang, Chengshi; Wen, Xin; Chen, Yang; Mao, Runyi; Cui, Danli; Li, Lan; Liu, Jingping; Chen, Younan; Cheng, Jun; Liu, Yanrong

doi:10.1111/jcmm.15250

Cited by 42 publications

(45 citation statements)

References 42 publications

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“…Matured DCs produce cytokines and costimulatory molecules and activate T lymphocytes and renal macrophages, thus mediating inflammation and kidney damage. Experimental immunomodulatory strategies, such as mesenchymal stem cell transplantation and Fms-like tyrosine kinase 3 inhibitor, reduce the population and maturation of DCs and ameliorate inflammation and CKD [55,56]. However, there is still limited information about the distinct functions of DCs' subsets in the pathogenesis of DN.…”

Section: Dendritic Cellsmentioning

confidence: 99%

Pathogenic Pathways and Therapeutic Approaches Targeting Inflammation in Diabetic Nephropathy

Rayego‐Mateos

Morgado‐Pascual

Opazo-Ríos

et al. 2020

IJMS

174

127

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Diabetic nephropathy (DN) is associated with an increased morbidity and mortality, resulting in elevated cost for public health systems. DN is the main cause of chronic kidney disease (CKD) and its incidence increases the number of patients that develop the end-stage renal disease (ESRD). There are growing epidemiological and preclinical evidence about the close relationship between inflammatory response and the occurrence and progression of DN. Several anti-inflammatory strategies targeting specific inflammatory mediators (cell adhesion molecules, chemokines and cytokines) and intracellular signaling pathways have shown beneficial effects in experimental models of DN, decreasing proteinuria and renal lesions. A number of inflammatory molecules have been shown useful to identify diabetic patients at high risk of developing renal complications. In this review, we focus on the key role of inflammation in the genesis and progression of DN, with a special interest in effector molecules and activated intracellular pathways leading to renal damage, as well as a comprehensive update of new therapeutic strategies targeting inflammation to prevent and/or retard renal injury.

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Section: Dendritic Cellsmentioning

confidence: 99%

Pathogenic Pathways and Therapeutic Approaches Targeting Inflammation in Diabetic Nephropathy

Rayego‐Mateos

Morgado‐Pascual

Opazo-Ríos

et al. 2020

IJMS

174

127

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“…For example, it has been shown that murine BM-MSCs induce the differentiation into regulatory DCs by HGF secretion ( Lu et al, 2019 ). Further functional data revealed that rat MSCs inhibit the maturation of CD103 + DCs, leading to a decreased ability to prime CD8 + T cells ( Zhang et al, 2020 ). Additionally, murine DCs that were treated with MSC-derived exosomes failed to stimulate T-cell proliferation upon LPS activation ( Shahir et al, 2020 ).…”

Section: Modulation Of Innate Immunity By Mscsmentioning

confidence: 99%

Immunomodulatory Properties of Mesenchymal Stromal Cells: An Update

Müller

Tunger

Wobus

et al. 2021

Front. Cell Dev. Biol.

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Mesenchymal stromal cells (MSCs) are characterized by an extraordinary capacity to modulate the phenotype and functional properties of various immune cells that play an essential role in the pathogenesis of inflammatory disorders. Thus, MSCs efficiently impair the phagocytic and antigen-presenting capacity of monocytes/macrophages and promote the expression of immunosuppressive molecules such as interleukin (IL)-10 and programmed cell death 1 ligand 1 by these cells. They also effectively inhibit the maturation of dendritic cells and their ability to produce proinflammatory cytokines and to stimulate potent T-cell responses. Furthermore, MSCs inhibit the generation and proinflammatory properties of CD4+ T helper (Th)1 and Th17 cells, while they promote the proliferation of regulatory T cells and their inhibitory capabilities. MSCs also impair the expansion, cytokine secretion, and cytotoxic activity of proinflammatory CD8+ T cells. Moreover, MSCs inhibit the differentiation, proliferation, and antibody secretion of B cells, and foster the generation of IL-10-producing regulatory B cells. Various cell membrane-associated and soluble molecules essentially contribute to these MSC-mediated effects on important cellular components of innate and adaptive immunity. Due to their immunosuppressive properties, MSCs have emerged as promising tools for the treatment of inflammatory disorders such as acute graft-versus-host disease, graft rejection in patients undergoing organ/cell transplantation, and autoimmune diseases.

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“…Dendritic cells (DCs) facilitate renal inflammation via promoting CD8+ T cell proliferation and activation during the development of CKD ( 124 , 125 ). Mechanistically, TGF-β1 promotes DCs accumulation in fibrotic tissue ( 126 ) and modulates DCs-mediated proliferation and activation of T cells ( 127 – 130 ), contributing to the imbalance between Th17 and Treg ( 131 ) and the interleukin 17 (IL-17) release from naive CD4 + cells ( 132 ).…”

Section: Tgf-β1 In Adaptive Immunity Of Ckdmentioning

confidence: 99%

TGF-β1 Signaling: Immune Dynamics of Chronic Kidney Diseases

et al. 2021

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Chronic kidney disease (CKD) is a major cause of morbidity and mortality worldwide, imposing a great burden on the healthcare system. Regrettably, effective CKD therapeutic strategies are yet available due to their elusive pathogenic mechanisms. CKD is featured by progressive inflammation and fibrosis associated with immune cell dysfunction, leading to the formation of an inflammatory microenvironment, which ultimately exacerbating renal fibrosis. Transforming growth factor β1 (TGF-β1) is an indispensable immunoregulator promoting CKD progression by controlling the activation, proliferation, and apoptosis of immunocytes via both canonical and non-canonical pathways. More importantly, recent studies have uncovered a new mechanism of TGF-β1 for de novo generation of myofibroblast via macrophage-myofibroblast transition (MMT). This review will update the versatile roles of TGF-β signaling in the dynamics of renal immunity, a better understanding may facilitate the discovery of novel therapeutic strategies against CKD.

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Mesenchymal stem cells alleviate rat diabetic nephropathy by suppressing CD103⁺ DCs‐mediated CD8⁺ T cell responses

Cited by 42 publications

References 42 publications

Pathogenic Pathways and Therapeutic Approaches Targeting Inflammation in Diabetic Nephropathy

Pathogenic Pathways and Therapeutic Approaches Targeting Inflammation in Diabetic Nephropathy

Immunomodulatory Properties of Mesenchymal Stromal Cells: An Update

TGF-β1 Signaling: Immune Dynamics of Chronic Kidney Diseases

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Mesenchymal stem cells alleviate rat diabetic nephropathy by suppressing CD103+ DCs‐mediated CD8+ T cell responses

Cited by 42 publications

References 42 publications

Pathogenic Pathways and Therapeutic Approaches Targeting Inflammation in Diabetic Nephropathy

Pathogenic Pathways and Therapeutic Approaches Targeting Inflammation in Diabetic Nephropathy

Immunomodulatory Properties of Mesenchymal Stromal Cells: An Update

TGF-β1 Signaling: Immune Dynamics of Chronic Kidney Diseases

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Product

Resources

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Mesenchymal stem cells alleviate rat diabetic nephropathy by suppressing CD103⁺ DCs‐mediated CD8⁺ T cell responses