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Special Issue "Th17 Cell in Autoimmune and Inflammatory Diseases"

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: closed (30 April 2017)

Special Issue Editor

Guest Editor
Dr. Shigeru Kotake

Tokyo Women's Medical University, Institute of Rheumatology, Tokyo, Japan
E-Mail
Interests: immunology, especially IL-17 and Th17, and bone cell biology, especially osteoclasts, in the pathogenesis of rheumatoid arthritis

Special Issue Information

Dear Colleagues,

The Th17 cell has become the most exiting field, not only in basic, but also clinical immunology. Th17 cells play an important role in bone cell biology. The anti-IL-17 antibody shows an effect on ankylosing spondylitis, non-radiographic axial spondylitis, psoriasis, and psoriatic arthritis. In therapy for rheumatoid arthritis (RA), anti-IL-17 antibody did not show enough effect in clinical trials. Recently, however, two meta-analysis reports demonstrated that the anti-IL-17 antibody is effective in ameliorating RA symptoms. Bi-specific antibodies, against both IL-17 and TNF-alpha, have shown effects on the activities of rheumatoid arthritis. In addition, the plasticity of Th17 is currently being investigated in basic and clinical immunology. The field of IL-17 and Th17 cells has moved very quickly, from bench to bedside or bedside to bench. Thus, please join us in presenting this Special Issue on the state-of-the-art research currently being performed worldwide, to investigate IL-17 and Th17, in order to help understand and treat various human autoimmune and inflammatory diseases.

Dr. Shigeru Kotake
Guest Editor

Manuscript Submission Information

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Keywords

  • Th17 cell
  • IL-17
  • rheumatoid arthritis
  • psoriasis
  • spondyloarthritis
  • bispecific antibody
  • osteoclast

Published Papers (7 papers)

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Review

Open AccessFeature PaperReview
IL-23 and Th17 Disease in Inflammatory Arthritis
J. Clin. Med. 2017, 6(9), 81; https://doi.org/10.3390/jcm6090081
Received: 29 April 2017 / Revised: 6 July 2017 / Accepted: 26 August 2017 / Published: 29 August 2017
Cited by 9 | PDF Full-text (722 KB) | HTML Full-text | XML Full-text
Abstract
IL-23, which is composed of p19 and p40 subunits, is a proinflammatory cytokine that contributes to the formation and maintenance of Th17 cells in inflammatory autoimmune diseases. IL-23 is a human osteoclastogenic cytokine and anti-IL-23 antibody attenuates paw volume and joint destruction in [...] Read more.
IL-23, which is composed of p19 and p40 subunits, is a proinflammatory cytokine that contributes to the formation and maintenance of Th17 cells in inflammatory autoimmune diseases. IL-23 is a human osteoclastogenic cytokine and anti-IL-23 antibody attenuates paw volume and joint destruction in CIA rats. IL-23 levels in serum and synovial fluid are high in rheumatoid arthritis (RA) patients, and IL-23 may be a useful biomarker for the diagnosis of RA. In addition, IL-23 affects the pathogenesis of inflammation and bone destruction through interaction with other cytokines such as IL-17 and TNF-α. Furthermore, polymorphisms of IL23R are a risk factor for ankylosing spondylitis (AS) and psoriatic arthritis (PsA), which indicates that IL-23 is also involved in the pathogenesis of spondyloarthritis (SpA). Finally, IL-17 and IL-23 inhibitors reduce the clinical manifestations of SpA. Thus, the IL-23/Th17 pathway is a therapeutic target for the treatment of inflammatory arthritis. Full article
(This article belongs to the Special Issue Th17 Cell in Autoimmune and Inflammatory Diseases)
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Open AccessFeature PaperReview
The Role of Th17 Cells in the Pathogenesis of Behcet’s Disease
J. Clin. Med. 2017, 6(7), 74; https://doi.org/10.3390/jcm6070074
Received: 27 April 2017 / Revised: 1 July 2017 / Accepted: 12 July 2017 / Published: 21 July 2017
Cited by 6 | PDF Full-text (206 KB) | HTML Full-text | XML Full-text
Abstract
Behcet’s disease (BD) is a polysymptomatic and recurrent systemic vasculitis with a chronic course and unknown cause. The pathogenesis of BD has not been fully elucidated; however, BD has been considered to be a typical Th1-mediated inflammatory disease, characterized by elevated levels of [...] Read more.
Behcet’s disease (BD) is a polysymptomatic and recurrent systemic vasculitis with a chronic course and unknown cause. The pathogenesis of BD has not been fully elucidated; however, BD has been considered to be a typical Th1-mediated inflammatory disease, characterized by elevated levels of Th1 cytokines such as IFN-γ, IL-2, and TNF-α. Recently, some studies reported that Th17-associated cytokines were increased in BD; thus, Th17 cells and the IL17/IL23 pathway may play important roles in the pathogenesis of BD. In this chapter, we focus on the pathogenic role of Th17 cells in BD. Full article
(This article belongs to the Special Issue Th17 Cell in Autoimmune and Inflammatory Diseases)
Open AccessFeature PaperReview
Th17 in Animal Models of Rheumatoid Arthritis
J. Clin. Med. 2017, 6(7), 73; https://doi.org/10.3390/jcm6070073
Received: 29 April 2017 / Revised: 13 July 2017 / Accepted: 15 July 2017 / Published: 21 July 2017
Cited by 9 | PDF Full-text (529 KB) | HTML Full-text | XML Full-text
Abstract
IL-17-secreting helper CD4 T cells (Th17 cells) constitute a newly identified subset of helper CD4 T cells that play a key role in the development of rheumatoid arthritis (RA) in its animal models. Recently, several models of spontaneous RA, which elucidate the mechanism [...] Read more.
IL-17-secreting helper CD4 T cells (Th17 cells) constitute a newly identified subset of helper CD4 T cells that play a key role in the development of rheumatoid arthritis (RA) in its animal models. Recently, several models of spontaneous RA, which elucidate the mechanism of RA onset, have been discovered. These animal models shed new light on the role of Th17 in the development of autoimmune arthritis. Th17 cells coordinate inflammation and promote joint destruction, acting on various cells, including neutrophils, macrophages, synovial fibroblasts, and osteoclasts. Regulatory T cells cannot control Th17 cells under conditions of inflammation. In this review, the pathogenic role of Th17 cells in arthritis development, which was revealed by the recent animal models of RA, is discussed. Full article
(This article belongs to the Special Issue Th17 Cell in Autoimmune and Inflammatory Diseases)
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Open AccessReview
Pathogenic Role of IL-17-Producing Immune Cells in Obesity, and Related Inflammatory Diseases
J. Clin. Med. 2017, 6(7), 68; https://doi.org/10.3390/jcm6070068
Received: 30 April 2017 / Revised: 3 July 2017 / Accepted: 4 July 2017 / Published: 14 July 2017
Cited by 21 | PDF Full-text (982 KB) | HTML Full-text | XML Full-text
Abstract
Obesity is associated with low-grade chronic inflammation. Indeed, adipose tissues (AT) in obese individuals are the former site of progressive infiltration by pro-inflammatory immune cells, which together with increased inflammatory adipokine secretion induce adipocyte insulin resistance. IL-17-producing T (Th17) cells are part of [...] Read more.
Obesity is associated with low-grade chronic inflammation. Indeed, adipose tissues (AT) in obese individuals are the former site of progressive infiltration by pro-inflammatory immune cells, which together with increased inflammatory adipokine secretion induce adipocyte insulin resistance. IL-17-producing T (Th17) cells are part of obese AT infiltrating cells, and are likely to be promoted by adipose tissue-derived mesenchymal stem cells, as previously reported by our team. Whereas Th17 cell are physiologically implicated in the neutralization of fungal and bacterial pathogens through activation of neutrophils, they may also play a pivotal role in the onset and/or progression of chronic inflammatory diseases, or cancer, in which obesity is recognized as a risk factor. In this review, we will highlight the pathogenic role of IL-17A producing cells in the mechanisms leading to inflammation in obesity and to progression of obesity-related inflammatory diseases. Full article
(This article belongs to the Special Issue Th17 Cell in Autoimmune and Inflammatory Diseases)
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Open AccessFeature PaperReview
The Plasticity of Th17 Cells in the Pathogenesis of Rheumatoid Arthritis
J. Clin. Med. 2017, 6(7), 67; https://doi.org/10.3390/jcm6070067
Received: 24 April 2017 / Revised: 28 June 2017 / Accepted: 2 July 2017 / Published: 10 July 2017
Cited by 14 | PDF Full-text (496 KB) | HTML Full-text | XML Full-text
Abstract
Helper T (Th) cells play an important role in the pathogenesis of autoimmune diseases, including rheumatoid arthritis (RA). It has been revealed that Th17 cells can shift to Th1 cells (i.e., “nonclassic Th1 cells”), which are reported to be more pathogenic than Th17 [...] Read more.
Helper T (Th) cells play an important role in the pathogenesis of autoimmune diseases, including rheumatoid arthritis (RA). It has been revealed that Th17 cells can shift to Th1 cells (i.e., “nonclassic Th1 cells”), which are reported to be more pathogenic than Th17 cells per se. Thus, the association of Th cells in the pathogenesis of autoimmune disease has become more complicated. We recently reported using peripheral blood from untreated and early-onset RA patients that the ratio of CD161+Th1 cells (i.e., Th17-derived Th1 cells to CD161+Th17 cells) is elevated and that levels of interferon-γ (IFNγ)+Th17 cells are inversely correlated with levels of anti-CCP antibodies. Here, we review the plasticity of Th17 cells in the pathogenesis of RA, suggesting possible implications for novel therapies. Full article
(This article belongs to the Special Issue Th17 Cell in Autoimmune and Inflammatory Diseases)
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Open AccessFeature PaperReview
T Helper 17 Cells in Primary Sjögren’s Syndrome
J. Clin. Med. 2017, 6(7), 65; https://doi.org/10.3390/jcm6070065
Received: 29 April 2017 / Revised: 23 June 2017 / Accepted: 27 June 2017 / Published: 5 July 2017
Cited by 7 | PDF Full-text (538 KB) | HTML Full-text | XML Full-text
Abstract
Primary Sjögren’s syndrome is an autoimmune disease characterized by diffuse infiltration of lymphocytes into exocrine glands and other tissues. The infiltrating lymphocytes have been identified as subsets of B cells and T cells, including T helper 17 cells, T regulatory cells and follicular [...] Read more.
Primary Sjögren’s syndrome is an autoimmune disease characterized by diffuse infiltration of lymphocytes into exocrine glands and other tissues. The infiltrating lymphocytes have been identified as subsets of B cells and T cells, including T helper 17 cells, T regulatory cells and follicular helper T cells. The role of these cells in the development of the syndrome is now known, as is their impact on the production of proinflammatory cytokines such as IL-6, IL-17, IL-22 and IL-23. In particular, experimental animal models and patients suggest that a shift in Th17/Treg balance toward the proinflammatory Th17 axis exacerbates primary Sjögren’s syndrome and other autoimmune disorders. Nevertheless, the pathogenesis of the disorder is not yet fully elucidated. This review summarizes the recent advances in therapeutic control of the Treg/Th17 balance, as well as the efficacy of candidate therapeutics against primary Sjögren’s syndrome. Full article
(This article belongs to the Special Issue Th17 Cell in Autoimmune and Inflammatory Diseases)
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Graphical abstract

Open AccessReview
Role of Gut Microbiota in Rheumatoid Arthritis
J. Clin. Med. 2017, 6(6), 60; https://doi.org/10.3390/jcm6060060
Received: 20 April 2017 / Revised: 1 June 2017 / Accepted: 6 June 2017 / Published: 9 June 2017
Cited by 21 | PDF Full-text (393 KB) | HTML Full-text | XML Full-text
Abstract
Rheumatoid arthritis (RA) is a systemic autoimmune disease, caused by both genetic and environmental factors. Recently, investigators have focused on the gut microbiota, which is thought to be an environmental agent affecting the development of RA. Here we review the evidence from animal [...] Read more.
Rheumatoid arthritis (RA) is a systemic autoimmune disease, caused by both genetic and environmental factors. Recently, investigators have focused on the gut microbiota, which is thought to be an environmental agent affecting the development of RA. Here we review the evidence from animal and human studies that supports the role of the gut microbiota in RA. We and others have demonstrated that the abundance of Prevotella copri is increased in some early RA. We have also used gnotobiotic experiments to show that dysbiosis in RA patients contributed to the development of Th17 cell-dependent arthritis in intestinal microbiota-humanized SKG mice. On the other hand, Prevotella histicola from human gut microbiota suppressed the development of arthritis. In summary, Prevotella species are involved in the pathogenesis of arthritis. Full article
(This article belongs to the Special Issue Th17 Cell in Autoimmune and Inflammatory Diseases)
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J. Clin. Med. EISSN 2077-0383 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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