ArticleScientific reports2017
Interleukin-17A is involved in mechanical hyperalgesia but not in the severity of murine antigen-induced arthritis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 52 citations in OpenAlex.
- IL-17 Stimulates Sensory Neurons and Sensitises Colonic Afferents to Noxious Stimuli in a PI3K Dependent Manner in Male Mice.Journal of neurochemistry · 2025Article
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- Concomitant Treatment with Doxycycline and Rifampicin in Balb/c Mice Infected withPharmaceuticals (Basel, Switzerland) · 2024Article
- Immune drivers of physiological and pathological pain.The Journal of experimental medicine · 2024Article
- Interleukin-17: A Putative Novel Pharmacological Target for Pathological Pain.Current neuropharmacology · 2024Review
- Circulating Inflammatory Biomarkers Predict Pain Change Following Exercise-Induced Shoulder Injury: Findings From the Biopsychosocial Influence on Shoulder Pain Preclinical Trial.The journal of pain · 2023Article
- Uncovering the Underworld of Axial Spondyloarthritis.International journal of molecular sciences · 2023Review
- Chronic Pain in Musculoskeletal Diseases: Do You Know Your Enemy?Journal of clinical medicine · 2022Review
- The Genesis of Pain in Osteoarthritis: Inflammation as a Mediator of Osteoarthritis Pain.Clinics in geriatric medicine · 2022Review
- The Neuroimmune Interplay in Joint Pain: The Role of Macrophages.Frontiers in immunology · 2022Review
- Interleukin-17 as a potential therapeutic target for chronic pain.Frontiers in immunology · 2022Review
- In-Depth Analysis of the Hidradenitis Suppurativa Serum Proteome Identifies Distinct Inflammatory Subtypes.The Journal of investigative dermatology · 2021Article
- IL-17: good fear no tears.Nature immunology · 2020Article
- TDAG8 deficiency reduces satellite glial number and pro-inflammatory macrophage number to relieve rheumatoid arthritis disease severity and chronic pain.Journal of neuroinflammation · 2020Article
- Temporal expression patterns of distinct cytokines and M1/M2 macrophage polarization regulate rheumatoid arthritis progression.Molecular biology reports · 2020Article
- MALT-1 mediates IL-17 neural signaling to regulate C. elegans behavior, immunity and longevity.Nature communications · 2020Article
- CD4European journal of immunology · 2020Article
- Pain Mechanism in Rheumatoid Arthritis: From Cytokines to Central Sensitization.Mediators of inflammation · 2020Review
- Therapeutic Efficacy of aFrontiers in microbiology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-17A (IL-17A) is considered an important pro-inflammatory cytokine but its importance in joint diseases such as rheumatoid arthritis (RA) is unclear. It has also been reported that IL-17A may induce pain but it is unclear whether pro-inflammatory and pro-nociceptive effects are linked. Here we studied in wild type (WT) and IL-17A knockout (IL-17AKO) mice inflammation and hyperalgesia in antigen-induced arthritis (AIA). We found that the severity and time course of AIA were indistinguishable in WT and IL-17AKO mice. Furthermore, the reduction of inflammation by sympathectomy, usually observed in WT mice, was preserved in IL-17AKO mice. Both findings suggest that IL-17A is redundant in AIA pathology. However, in the course of AIA IL-17AKO mice showed less mechanical hyperalgesia than WT mice indicating that IL-17A contributes to pain even if it is not crucial for arthritis pathology. In support for a role of IL-17A and other members of the IL-17 family in the generation of pain we found that sensory neurones in the dorsal root ganglia (DRG) express all IL-17 receptor subtypes. Furthermore, in isolated DRG neurones most IL-17 isoforms increased tetrodotoxin- (TTX-) resistant sodium currents which indicate a role of IL-17 members in inflammation-evoked sensitization of sensory nociceptive neurones.
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