Decoy receptor 3 protects non-obese diabetic mice from autoimmune diabetes by regulating dendritic cell maturation and function

Wang, Aline Yen Ling; Chou, Feng-Cheng; Sung, Hsiang-Hsuan; Fan, Pao‐Luo; Hsueh, Chao-Wen; Lin, Wen‐Chi; Chen, Shyi-Jou; Lin, Wan-Wan; Sytwu, Huey‐Kang

doi:10.1016/j.molimm.2010.07.001

Cited by 13 publications

(12 citation statements)

References 45 publications

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“…We can confidently say that IFNβ, GA, and mitoxantrone are fairly clinically effective for MS patients. The addition of estrogen(s) or minocycline has also shown benefits in the treatment of MS. We have established the protective effects of DcR3 and EPO against EAE [174,181], but further evidence is required before they can be used clinically for the treatment of MS. More immunomodulatory therapeutic agents are currently in clinical trials, including fingolimod (FTY720), alemtuzumab, and rituximab add-on therapies [182]. The extensive clinical application of these potential novel immunomodulatory therapeutic agents will be under close scrutiny in the near future.…”

Section: Discussionmentioning

confidence: 99%

Current Status of the Immunomodulation and Immunomediated Therapeutic Strategies for Multiple Sclerosis

Chen

Wang

Fan

et al. 2012

Clinical and Developmental Immunology

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Multiple sclerosis (MS) is an autoimmune disease of the central nervous system, and CD4+ T cells form the core immunopathogenic cascade leading to chronic inflammation. Traditionally, Th1 cells (interferon-γ-producing CD4+ T cells) driven by interleukin 12 (IL12) were considered to be the encephalitogenic T cells in MS and experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Currently, Th17 cells (Il17-producing CD4+ T cells) are considered to play a fundamental role in the immunopathogenesis of EAE. This paper highlights the growing evidence that Th17 cells play the core role in the complex adaptive immunity of EAE/MS and discusses the roles of the associated immune cells and cytokines. These constitute the modern immunological basis for the development of novel clinical and preclinical immunomodulatory therapies for MS discussed in this paper.

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Section: Discussionmentioning

confidence: 99%

Current Status of the Immunomodulation and Immunomediated Therapeutic Strategies for Multiple Sclerosis

Chen

Wang

Fan

et al. 2012

Clinical and Developmental Immunology

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“…Accordingly, the effects of 4 weeks of DcR3 Fc protein (DcR3a) (30 mg/kg body weight, twice per week) or human IgFc (control group) i.p. on the progression of SS to NASH was evaluated in another group of DcR3a + WT NASH mice . Body weight and food intake were recorded weekly throughout the experiments.…”

Section: Methodsmentioning

confidence: 99%

“…on the progression of SS to NASH was evaluated in another group of DcR3a + WT NASH mice. 20 Body weight and food intake were recorded weekly throughout the experiments. Food intake was measured by weighing the pellets once per week.…”

Section: Animals Genetic Dcr3 Replacement Treatment In Transgenic Micementioning

confidence: 99%

Mechanisms of the prevention and inhibition of the progression and development of non‐alcoholic steatohepatitis by genetic and pharmacological decoy receptor 3 supplementation

Lee

Yang

Wang

et al. 2017

Hepatology Research

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“…DcR3 is not found in mouse genome, suggesting that additional complexity of TL1A-DR3 pathway in human as compared to mouse. DcR3 protects the development of autoimmune diabetes [91, 92], IgA nephropathy [93], and crescent glomerulonephritis [94] model mice, while DcR3-transgenic mice develop SLE-like syndrome [95]. These reports suggest that DcR3 also plays an important role in the pathogenesis of autoimmune and inflammatory diseases.…”

Section: The Association Of Dcr3 With Autoimmune and Inflammatory mentioning

confidence: 99%

The Role of TL1A and DR3 in Autoimmune and Inflammatory Diseases

Aiba

Nakamura

2013

Mediators of Inflammation

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TNF-like ligand 1A (TL1A), which binds its cognate receptor DR3 and the decoy receptor DcR3, is an identified member of the TNF superfamily. TL1A exerts pleiotropic effects on cell proliferation, activation, and differentiation of immune cells, including helper T cells and regulatory T cells. TL1A and its two receptors expression is increased in both serum and inflamed tissues in autoimmune diseases such as inflammatory bowel disease (IBD), rheumatoid arthritis (RA), and ankylosing spondylitis (AS). Polymorphisms of the TNFSF15 gene that encodes TL1A are associated with the pathogenesis of irritable bowel syndrome, leprosy, and autoimmune diseases, including IBD, AS, and primary biliary cirrhosis (PBC). In mice, blocking of TL1A-DR3 interaction by either antagonistic antibodies or deletion of the DR3 gene attenuates the severity of multiple autoimmune diseases, whereas sustained TL1A expression on T cells or dendritic cells induces IL-13-dependent small intestinal inflammation. This suggests that modulation of TL1A-DR3 interaction may be a potential therapeutic target in several autoimmune diseases, including IBD, RA, AS, and PBC.

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Decoy receptor 3 protects non-obese diabetic mice from autoimmune diabetes by regulating dendritic cell maturation and function

Cited by 13 publications

References 45 publications

Current Status of the Immunomodulation and Immunomediated Therapeutic Strategies for Multiple Sclerosis

Current Status of the Immunomodulation and Immunomediated Therapeutic Strategies for Multiple Sclerosis

Mechanisms of the prevention and inhibition of the progression and development of non‐alcoholic steatohepatitis by genetic and pharmacological decoy receptor 3 supplementation

The Role of TL1A and DR3 in Autoimmune and Inflammatory Diseases

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