IL-33 is a member of the IL-1 family of cytokines whose role remains controversial in rheumatoid arthritis (RA). The present study was performed to evaluate the correlation of IL-33 with other cytokines and chemokines in serum and the synovia, and to explore the nature of the association. The concentration of IL-33 in samples from 96 patients with RA was analyzed. The response of fibroblast-like synoviocytes (FLSs) to treatment with different concentrations of IL-33 was assessed . IL-33 was indicated to exhibit an association with multiple cytokines and chemokines in synovial fluid with an inverted-U-shaped trend, including IL-6, IL-1β, IL-8, MIG and IP-10, but not in the serum. Furthermore, experiments confirmed that IL-33 also exerted a U-type dose-dependent regulatory effect on FLS function. In addition, the data-points do not exactly follow the U-shaped curve fit in most cases, therefore, the applicability of this mathematical model in clinical practice is limited.
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http://dx.doi.org/10.3892/etm.2020.9592 | DOI Listing |
Arthritis Res Ther
January 2025
Department of Biomedical Sciences, Humanitas University, Via R Levi Montalcini 4, Pieve Emanuele, Milan, 20090, Italy.
Background: There is still a significant proportion of patients with rheumatoid arthritis (RA) in whom multiple therapeutic lines are ineffective. These cases are defined by the EULAR criteria as Difficult-to-Treat RA (D2T-RA) for which there is limited knowledge of predisposing factors.
Objective: To identify the clinical features associated with D2T-RA in real-life practice.
Nat Genet
January 2025
Department of Statistical Genetics, Osaka University Graduate School of Medicine, Suita, Japan.
Aberrant immune responses to viral pathogens contribute to pathogenesis, but our understanding of pathological immune responses caused by viruses within the human virome, especially at a population scale, remains limited. We analyzed whole-genome sequencing datasets of 6,321 Japanese individuals, including patients with autoimmune diseases (psoriasis vulgaris, rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), pulmonary alveolar proteinosis (PAP) or multiple sclerosis) and coronavirus disease 2019 (COVID-19), or healthy controls. We systematically quantified two constituents of the blood DNA virome, endogenous HHV-6 (eHHV-6) and anellovirus.
View Article and Find Full Text PDFJ Hand Ther
January 2025
Faculty of Health and Life Sciences, University of Exeter, Exeter, United Kingdom.
Background: The Strengthening and Stretching for Rheumatoid Arthritis of the Hand (SARAH) program is an evidence-based exercise program for adults with hand function difficulties due to rheumatoid arthritis. A self-guided online version of the program has been developed for direct access by patients.
Purpose: To evaluate the delivery of the online program in routine therapy care and its impact on clinical outcomes, before making it widely available.
Inflammopharmacology
January 2025
Department of Food Technology and Nutrition, Lovely Professional University, Phagwara, Punjab, 144411, India.
Rheumatoid Arthritis (RA) is an autoimmune, chronic, systemic inflammatory disease that causes redness, swelling, stiffness, and joint pain. It is a long-lasting disease that can have a widespread impact on the body, often affecting the hands, feet, and wrists. The immune cells, such as dendritic cells, T cells, B cells, macrophages, and neutrophils, play a significant role in bone degradation and inflammation.
View Article and Find Full Text PDFExp Cell Res
January 2025
Department of Plastic Surgery, The First Affiliated Hospital of Anhui Medical University, Anhui 230032, China. Electronic address:
Keloids are disfiguring proliferative scars, and their pathological mechanisms are still unclear. We have previously established that FoxC1 plays a significant role in rheumatoid arthritis and osteoarthritis, but its molecular mechanisms in pathological scar formation remain elusive. In this study, we analyzed keloid tissue characteristics using HE staining and immunohistochemistry, revealing abnormal expression of FoxC1 and Notch3 in keloids.
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