Interleukin-10 attenuation of collagen-induced arthritis is associated with suppression of interleukin-17 and retinoid-related orphan receptor γt production in macrophages and repression of classically activated macrophages

Liang, Ye; Wen, Zhongyang; Li, Yanqun; Chen, Bingni; Yu, Ting; Liu, Lanying; Zhang, Jinshun; Ma, Yanbing; Xiao, Shuying; Ding, Liping; Li, L i; Huang, Zhong

doi:10.1186/ar4544

Cited by 57 publications

(49 citation statements)

References 49 publications

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“…In line with this study, it was shown that IL-10 knock-out mice develop exacerbated CIA and that the phenotype of synovial macrophages in these animals corresponds mainly to proinflammatory M1-like macrophages [35]. Moreover, in response to TNF- α and IL-1 β , activated synovial fibroblasts produce high levels of receptor activator of nuclear factor- κ B (NF- κ B) ligand (RANKL) and macrophage colony-stimulating factor 1 (M-CSF) which are essential for formation of osteoclasts by fusion of myeloid precursors of monocytes/macrophages [36–38].…”

Section: Innate Immunity In Ra and The Effect Of Mscssupporting

confidence: 65%

Mesenchymal Stem Cells Regulate the Innate and Adaptive Immune Responses Dampening Arthritis Progression

Contreras-López

Figueroa

Djouad

et al. 2016

Stem Cells International

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Mesenchymal stem cells (MSCs) are multipotent stem cells that are able to immunomodulate cells from both the innate and the adaptive immune systems promoting an anti-inflammatory environment. During the last decade, MSCs have been intensively studied in vitro and in vivo in experimental animal model of autoimmune and inflammatory disorders. Based on these studies, MSCs are currently widely used for the treatment of autoimmune diseases such as rheumatoid arthritis (RA) characterized by complex deregulation of the immune systems. However, the therapeutic properties of MSCs in arthritis are still controverted. These controversies might be due to the diversity of MSC sources and isolation protocols used, the time, the route and dose of MSC administration, the variety of the mechanisms involved in the MSCs suppressive effects, and the complexity of arthritis pathogenesis. In this review, we discuss the role of the interactions between MSCs and the different immune cells associated with arthritis pathogenesis and the possible means described in the literature that could enhance MSCs therapeutic potential counteracting arthritis development and progression.

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Section: Innate Immunity In Ra and The Effect Of Mscssupporting

confidence: 65%

Mesenchymal Stem Cells Regulate the Innate and Adaptive Immune Responses Dampening Arthritis Progression

Contreras-López

Figueroa

Djouad

et al. 2016

Stem Cells International

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“…We used cellspecific markers NOS2 and CD206 as representatives of M1 and M2 cells, respectively. Others have used these markers to investigate M1 and M2 subsets in murine models of arthritis and carditis (30)(31)(32). Using these markers, we were able to phenotype M1 (F4/ 80 ϩ NOS2 ϩ CD206 Ϫ ) and M2 (F4/80 ϩ NOS2 Ϫ CD206 ϩ ) macrophages within the joints and hearts of Borrelia-infected mice at a number of key time points.…”

Section: Discussionmentioning

confidence: 86%

“…2A. M1 macrophages were defined by their expression of NOS2, and M2 macrophages were defined by their expression of CD206 as reported by others (30)(31)(32). Following infection, arthritis development was monitored by measuring ankle swelling over the course of about 2 months (Fig.…”

Section: Lasky Et Almentioning

confidence: 99%

Macrophage Polarization during Murine Lyme Borreliosis

2015

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Infection of C3H mice with Borrelia burgdorferi, the causative agent of Lyme disease, reliably produces an infectious arthritis and carditis that peak around 3 weeks postinfection and then spontaneously resolve. Macrophage polarization has been suggested to drive inflammation, the clearance of bacteria, and tissue repair and resolution in a variety of infectious disease models. During Lyme disease it is clear that macrophages are capable of clearing Borrelia spirochetes and exhausted neutrophils; however, the role of macrophage phenotype in disease development or resolution has not been studied. Using classical (NOS2) and alternative (CD206) macrophage subset-specific markers, we determined the phenotype of F4/80 ؉ macrophages within the joints and heart throughout the infection time course. Within the joint, CD206؉ macrophages dominated throughout the course of infection, and NOS2؉ macrophage numbers became elevated only during the peak of inflammation. We also found dual NOS2 ؉ CD206 ؉ macrophages which increased during resolution. In contrast to findings for the ankle joints, numbers of NOS2 ؉ and CD206؉ macrophages in the heart were similar at the peak of inflammation. 5-Lipoxygenase-deficient (5-LOX ؊/؊ ) mice, which display a failure of Lyme arthritis resolution, recruited fewer F4/80 ؉ cells to the infected joints and heart, but macrophage subset populations were unchanged. These results highlight differences in the inflammatory infiltrates during Lyme arthritis and carditis and demonstrate the coexistence of multiple macrophage subsets within a single inflammatory site. Macrophages play a dynamic role in the immune system as both inflammatory and anti-inflammatory mediators. Their phenotype is highly flexible and dependent upon the cytokine stimulus of the microenvironment they infiltrate (1). They are routinely classified as proinflammatory and immunomodulatory (M1) or anti-inflammatory and remodeling (M2) macrophages, but their phenotype actually lies within a spectrum of inflammatory to anti-inflammatory polarization (2). The language within the field is currently being modified to ensure that the macrophages being studied have a clear phenotypic description, and we use the nomenclature recently suggested (3). Within the last 15 years, much work has been done to phenotypically characterize macrophage subsets. Identifying unique surface and intracellular markers, as well as understanding transcriptional regulation, has allowed the importance of specific macrophage phenotypes in infectious and autoimmune models to be uncovered.Classically activated M1 macrophages are proinflammatory cells capable of destroying pathogens, tumor cells, and various foreign compounds. Stimulation of undifferentiated macrophages with lipopolysaccharide (LPS) and gamma interferon (IFN-␥), or tumor necrosis factor alpha (TNF-␣), induces polarization to the M1 phenotype (4, 5). They can be recognized both in vitro and in vivo by the production of nitric oxide species (NOS), as well as other proinflammatory molecules, including ...

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“…Synovial tissues, joint cells, and synovial fluids were collected according to a previously described protocol (18). Synovial fluid samples were stored at 280˚C prior to assay.…”

Section: Preparation Of Synovial Tissues and Joint Cells And Collectimentioning

confidence: 99%

“…Tissue sections were prepared and stained with H&E. Histopathologic scoring of joint damage was performed under blinded conditions, according to a widely used scoring system for evaluating synovitis, cartilage degradation, and bone erosion (18).…”

Section: Histopathologic Analysismentioning

confidence: 99%

IL-37 Alleviates Rheumatoid Arthritis by Suppressing IL-17 and IL-17–Triggering Cytokine Production and Limiting Th17 Cell Proliferation

Ye¹,

Jiang²,

Deng

et al. 2015

The Journal of Immunology

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140

127

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IL-37, a new member of the IL-1 cytokine family, is a natural inhibitor of innate immunity associated with autoimmune diseases. This study was undertaken to evaluate whether IL-37 has antiarthritic effects in patients with rheumatoid arthritis (RA) and in mice with collagen-induced arthritis (CIA). In this study, we analyzed the expression of IL-37 in PBMCs, serum, and lymphocytes from RA patients as well as CD4+ T cells polarized under Th1/Th2/Th17 conditions. The role of IL-37 was assessed by investigating the effects of recombinant human (rh)IL-37 and an adenovirus encoding human IL-37 (Ad–IL-37) on Th17 cells and Th17-related cytokines in RA patients and CIA mice. We found that active RA patients showed higher IL-37 levels compared with patients with inactive RA and healthy controls. Upregulated IL-37 expression also was found in CD3+ T cells and CD4+ T cells from RA patients and in Th1/Th17-differentiation conditions. rhIL-37 markedly decreased IL-17 expression and Th17 cell frequency in PBMCs and CD4+ T cells from RA patients. Furthermore, IL-37 exerted a more suppressive effect on Th17 cell proliferation, whereas it had little or no effect on Th17 cell differentiation. IL-17 and IL-17–driving cytokine production were significantly reduced in synovium and joint cells from CIA mice receiving injections of Ad–IL-37. Our findings indicate that IL-37 plays a potent immunosuppressive role in the pathogenesis of human RA and CIA models via the downregulation of IL-17 and IL-17–triggering cytokine production and the curbing of Th17 cell proliferation.

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Interleukin-10 attenuation of collagen-induced arthritis is associated with suppression of interleukin-17 and retinoid-related orphan receptor γt production in macrophages and repression of classically activated macrophages

Cited by 57 publications

References 49 publications

Mesenchymal Stem Cells Regulate the Innate and Adaptive Immune Responses Dampening Arthritis Progression

Mesenchymal Stem Cells Regulate the Innate and Adaptive Immune Responses Dampening Arthritis Progression

Macrophage Polarization during Murine Lyme Borreliosis

IL-37 Alleviates Rheumatoid Arthritis by Suppressing IL-17 and IL-17–Triggering Cytokine Production and Limiting Th17 Cell Proliferation

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