IL-17A exacerbates synovial inflammation in osteoarthritis via activation of endoplasmic reticulum stress.

IF 4.8 2区医学 Q2 IMMUNOLOGY

International immunopharmacology Pub Date : 2025-01-03 Epub Date: 2024-12-10 DOI:10.1016/j.intimp.2024.113733

Wen Sun, Xueyan Li, Liyuan Zhang, Yuheng Zhang, Yi Shi, Huaqiang Tao, Jing Zhou, Yuefeng Hao, Guangdong Chen, Chengyong Gu, Xing Yang

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引用次数: 0

Abstract

The primary clinical manifestations of osteoarthritis (OA) are joint pain and restricted movement capabilities. Synovial inflammation, serving as an initiator of OA progression, intensifies cartilage damage via the generation of various deleterious agents, including pro-inflammatory cytokines and nociceptive mediators. Despite extensive research on modulating synovial inflammation to retard OA progression, the underlying pathophysiological mechanisms of synovial inflammation in OA remain elusive. Interleukin-17A (IL-17A), a pro-inflammatory cytokine released by activated T lymphocytes, is a therapeutic target for numerous inflammatory and autoimmune pathologies. This study investigates the role and mechanism of IL-17A in OA synovial inflammation using both in vivo and in vitro models and examines the impact of the endoplasmic reticulum stress (ERS) inhibitor, 4-Phenylbutyric Acid (4-PBA). Our findings indicate that IL-17A may be implicated in synovial inflammation through ERS and suggest a potential therapeutic direction for mitigating synovial inflammation in OA.

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来源期刊

International immunopharmacology 医学-免疫学

CiteScore

8.40

自引率

3.60%

发文量

935

审稿时长

53 days

期刊介绍： International Immunopharmacology is the primary vehicle for the publication of original research papers pertinent to the overlapping areas of immunology, pharmacology, cytokine biology, immunotherapy, immunopathology and immunotoxicology. Review articles that encompass these subjects are also welcome. The subject material appropriate for submission includes: • Clinical studies employing immunotherapy of any type including the use of: bacterial and chemical agents; thymic hormones, interferon, lymphokines, etc., in transplantation and diseases such as cancer, immunodeficiency, chronic infection and allergic, inflammatory or autoimmune disorders. • Studies on the mechanisms of action of these agents for specific parameters of immune competence as well as the overall clinical state. • Pre-clinical animal studies and in vitro studies on mechanisms of action with immunopotentiators, immunomodulators, immunoadjuvants and other pharmacological agents active on cells participating in immune or allergic responses. • Pharmacological compounds, microbial products and toxicological agents that affect the lymphoid system, and their mechanisms of action. • Agents that activate genes or modify transcription and translation within the immune response. • Substances activated, generated, or released through immunologic or related pathways that are pharmacologically active. • Production, function and regulation of cytokines and their receptors. • Classical pharmacological studies on the effects of chemokines and bioactive factors released during immunological reactions.