ArticleArthritis & rheumatology (Hoboken, N.J.)2014
ES-62 protects against collagen-induced arthritis by resetting interleukin-22 toward resolution of inflammation in the joints.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 54 citations in OpenAlex.
- SIK inhibitor HG-9-91-01 suppresses the pathogenic activity of fibroblast-like synoviocytes in rheumatoid arthritis.RMD open · 2026Article
- Inhibition of Aberrant Activated Fibroblast-Like Synoviocytes in Rheumatoid Arthritis by Leishmania Peptide via the Regulation of Fatty Acid Synthesis Metabolism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Undenatured type II collagen protects against collagen-induced arthritis by restoring gut-joint homeostasis and immunity.Communications biology · 2024Article
- Epigenetic changes induced by parasitic worms and their excretory-secretory products.Biochemical Society transactions · 2024Review
- The parasitic worm product ES-62 protects against collagen-induced arthritis by resetting the gut-bone marrow axis in a microbiome-dependent manner.Frontiers in tropical diseases · 2024Article
- Gut-joint axis: Gut dysbiosis can contribute to the onset of rheumatoid arthritisFrontiers in cellular and infection microbiology · 2023Review
- Synovial Fibroblast Sialylation Regulates Cell Migration and Activation of Inflammatory Pathways in Arthritogenesis.Frontiers in immunology · 2022Article
- Suppression of inflammatory arthritis by the parasitic worm product ES-62 is associated with epigenetic changes in synovial fibroblasts.PLoS pathogens · 2021Article
- Modification of Gut Microbiota in Inflammatory Arthritis: Highlights and Future Challenges.Current rheumatology reports · 2021Review
- Loss of α2-6 sialylation promotes the transformation of synovial fibroblasts into a pro-inflammatory phenotype in arthritis.Nature communications · 2021Article
- Systemic overexpression of interleukin-22 induces the negative immune-regulator SOCS3 and potently reduces experimental arthritis in mice.Rheumatology (Oxford, England) · 2021Article
- Interleukin-22 and connective tissue diseases: emerging role in pathogenesis and therapy.Cell & bioscience · 2021Review
- The parasitic worm product ES-62 normalises the gut microbiota bone marrow axis in inflammatory arthritis.Nature communications · 2019Article
- Anti-inflammatory and immune-regulatory cytokines in rheumatoid arthritis.Nature reviews. Rheumatology · 2019Review
- Failure of the Anti-Inflammatory Parasitic Worm Product ES-62 to Provide Protection in Mouse Models of Type I Diabetes, Multiple Sclerosis, and Inflammatory Bowel Disease.Molecules (Basel, Switzerland) · 2018Article
- Innate lymphoid cells in autoimmunity and chronic inflammatory diseases.Seminars in immunopathology · 2018Review
- Small Molecule Analogues of the parasitic worm product ES-62 interact with the TIR domain of MyD88 to inhibit pro-inflammatory signalling.Scientific reports · 2018Article
- Protection Against Arthritis by the Parasitic Worm Product ES-62, and Its Drug-Like Small Molecule Analogues, Is Associated With Inhibition of Osteoclastogenesis.Frontiers in immunology · 2018Article
- Dendritic cells provide a therapeutic target for synthetic small molecule analogues of the parasitic worm product, ES-62.Scientific reports · 2017Article
- Increased expression of Th17 cytokines and interleukin-22 correlates with disease activity in pristane-induced arthritis in rats.PloS one · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveThe parasitic worm-derived immunomodulator ES-62 protects against disease in the mouse collagen-induced arthritis (CIA) model of rheumatoid arthritis (RA) by suppressing pathogenic interleukin-17 (IL-17) responses. The Th17-associated cytokine IL-22 also appears to have a pathogenic role in autoimmune arthritis, particularly in promoting proinflammatory responses by synovial fibroblasts and osteoclastogenesis. The present study was undertaken to investigate whether the protection against joint damage afforded by ES-62 also reflects suppression of IL-22.
methodsThe role(s) of IL-22 was assessed by investigating the effects of neutralizing anti-IL-22 antibodies and recombinant IL-22 (rIL-22) on proinflammatory cytokine production, synovial fibroblast responses, and joint damage in mice with CIA in the presence or absence of ES-62.
resultsNeutralization of IL-22 during the initiation phase abrogated CIA, while administration of rIL-22 enhanced synovial fibroblast responses and exacerbated joint pathology. In contrast, after disease onset anti-IL-22 did not suppress progression, whereas administration of rIL-22 promoted resolution of inflammation. Consistent with these late antiinflammatory effects, the protection afforded by ES-62 was associated with elevated levels of IL-22 in the serum and joints that reflected a desensitization of the synovial fibroblast responses. Moreover, neutralization of IL-22 during the late effector stage of disease prevented ES-62-mediated desensitization of synovial fibroblast responses and protection against CIA.
conclusionIL-22 plays a dual role in CIA, being pathogenic during the initiation phase while acting to resolve inflammation and joint damage during established disease. Harnessing of the tissue repair properties of IL-22 by ES-62 highlights the potential for joint-targeted therapeutic modulation of synovial fibroblast responses and consequent protection against bone damage in RA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.