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Arthritis and Inflammatory Cytokine 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 3398

Special Issue Editor


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Guest Editor
Division of Rheumatology, Department of Internal Medicine, Yeouido St. Mary's Hospital, Catholic University of Korea, Seoul, Republic of Korea
Interests: rheumatoid arthritis; osteoarthritis; autoimmunity; nociceptive pathway; Th17 cells; regulatory T-cells; inflammatory cytokine; synovitis; chondrocytes; lupus nephritis
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Special Issue Information

Dear Colleagues,

Inflammatory cytokines are involved in the development and progression of various autoimmune-mediated arthritis such as rheumatoid arthritis and psoriatic arthritis. The pathophysiological significance of inflammatory cytokines and their related pathways has been found to be reliable in inflammatory arthritis through many previous studies, leading to the development of successful cytokine-targeting strategies, such as TNFα or IL-17.

This Special Issue aims to stimulate comprehensive research that confirms the previously unknown roles of inflammatory cytokines in autoimmune arthritis through preclinical animal models and/or patient-derived samples, suggesting their potential as a diagnostic or therapeutic strategy. The Special Issue wants to focus on both basic science and translational research in inflammatory arthritis.

Since inflammatory cytokines act in various ways for each disease, it is better to specify one disease in each study. Of course, other inflammatory diseases can be used as a control for comparison. It is not advisable to prove the roles of specific inflammatory cytokines in the inflammatory environment by collecting a variety of inflammatory arthritis.

Dr. Su-Jin Moon
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Keywords

  • rheumatoid arthritis
  • osteoarthritis
  • inflammatory cytokine
  • chondrocytes
  • T-cells
  • B-cells
  • macrophages
  • nociceptive pathway

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Published Papers (2 papers)

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Research

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15 pages, 2916 KiB  
Article
Changes in Inflammatory Cytokines in Responders and Non-Responders to TNFα Inhibitor and IL-17A Inhibitor: A Study Examining Psoriatic Arthritis Patients
by Marie Skougaard, Magnus Friis Søndergaard, Sisse Bolm Ditlev and Lars Erik Kristensen
Int. J. Mol. Sci. 2024, 25(5), 3002; https://doi.org/10.3390/ijms25053002 - 05 Mar 2024
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Abstract
This study aimed to examine the changes in biomarker levels in responders and non-responders to tumor necrosis factor alpha inhibitor (TNFi) and interleukin-17A inhibitor (IL-17Ai) in psoriatic arthritis (PsA) patients over a 4-month period after treatment initiation. A total of 68 PsA patients [...] Read more.
This study aimed to examine the changes in biomarker levels in responders and non-responders to tumor necrosis factor alpha inhibitor (TNFi) and interleukin-17A inhibitor (IL-17Ai) in psoriatic arthritis (PsA) patients over a 4-month period after treatment initiation. A total of 68 PsA patients initiating either TNFi, IL-17Ai, or methotrexate treatment were included. Blood plasma and clinical outcome measures were collected adjacent to treatment initiation and after four months. A commercially available multiplex immunoassay was included to evaluate 54 biomarkers. Mean changes were used to evaluate change over time. A statistically significant decrease in pro-inflammatory cytokines IL-6 (log-transformed mean change −0.97, 95%CI −4.30; 2.37, [p = 0.032]) and an increase in anti-inflammatory IL-10 (0.38, 95%CI 1.74; 2.50 [p = 0.010]) were seen in TNFi responders. Meanwhile, a statistically significant increase in the target cytokine IL-17A was seen in both IL-17Ai responders (2.49, 95%CI −1.84; 6.85 [p = 0.031]) and non-responders (2.48, 95%CI −1.46; 6.41 [p = 0.001]). This study demonstrated differing changes in cytokine levels when comparing treatment responders and non-responders, highlighting the need to improve the understanding of the different immune response mechanisms explaining different responses to medical treatment in PsA patients. Full article
(This article belongs to the Special Issue Arthritis and Inflammatory Cytokine 2.0)
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Review

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20 pages, 1676 KiB  
Review
Inflammatory Cytokines in Psoriatic Arthritis: Understanding Pathogenesis and Implications for Treatment
by Bong-Woo Lee and Su-Jin Moon
Int. J. Mol. Sci. 2023, 24(14), 11662; https://doi.org/10.3390/ijms241411662 - 19 Jul 2023
Cited by 7 | Viewed by 2435
Abstract
Psoriatic arthritis (PsA) is a persistent, inflammatory disease that affects individuals with psoriasis, arthritis, and enthesitis. Research has demonstrated that inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-23 (IL-23), and interleukin-17 (IL-17) play a pivotal role in both the onset and progression [...] Read more.
Psoriatic arthritis (PsA) is a persistent, inflammatory disease that affects individuals with psoriasis, arthritis, and enthesitis. Research has demonstrated that inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-23 (IL-23), and interleukin-17 (IL-17) play a pivotal role in both the onset and progression of PsA. These cytokines are generated by activated immune cells and stimulate the attraction of inflammatory cells to the synovium and joint tissues, resulting in the deterioration of cartilage and bone. The blocking of these cytokines has become a successful treatment strategy for PsA, as biological drugs that inhibit TNF-α, IL-23, and IL-17 have demonstrated notable clinical benefits. The association between PsA and other types of inflammatory cytokines or chemokines, excluding TNF-α, IL-23, and IL-17, has been extensively investigated in numerous studies. These findings may provide a chance for the discovery of novel therapeutic agents targeting other molecules, distinct from the currently approved biologics and targeted synthetic disease-modifying anti-rheumatic drugs. In this review, we discuss the current understanding of the role of inflammatory cytokines in PsA pathogenesis and clinical implications of targeting these cytokines for PsA treatment. Full article
(This article belongs to the Special Issue Arthritis and Inflammatory Cytokine 2.0)
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