ArticleArthritis research & therapy2015
Joint production of IL-22 participates in the initial phase of antigen-induced arthritis through IL-1β production.
Article in Arthritis research & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Effect of sleep loss on pain-New conceptual and mechanistic avenues.Frontiers in neuroscience · 2022Pooled it
- Review
- Resveratrol Attenuates Rheumatoid Arthritis Induce Neutrophil Extracellular Traps via TLR-4 Mediated Inflammation in C57BL/6 Mice.Physiological research · 2024Article
- Artemisinin inhibits neutrophil and macrophage chemotaxis, cytokine production and NET release.Scientific reports · 2022Article
- Nanobodies dismantle post-pyroptotic ASC specks and counteract inflammation in vivo.EMBO molecular medicine · 2022Article
- Methotrexate promotes recovery of arthritis-induced alveolar bone loss and modifies the composition of the oral-gut microbiota.Anaerobe · 2022Article
- The emerging role of neutrophils in autoimmune-associated disorders: effector, predictor, and therapeutic targets.MedComm · 2021Review
- Aryl hydrocarbon receptor (Ahr)-dependent Il-22 expression by type 3 innate lymphoid cells control of acute joint inflammation.Journal of cellular and molecular medicine · 2021Article
- Systemic overexpression of interleukin-22 induces the negative immune-regulator SOCS3 and potently reduces experimental arthritis in mice.Rheumatology (Oxford, England) · 2021Article
- Effect of Shujin Xiaotong capsules combined with ultrashort wave therapy on pain and inflammatory cytokines in patients with chronic knee osteoarthritis.American journal of translational research · 2021Article
- IL-22 Promotes IFN-γ-Mediated Immunity againstBiomolecules · 2020Article
- Thirty days after anterior cruciate ligament transection is sufficient to induce signs of knee osteoarthritis in rats: pain, functional impairment, and synovial inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- Innate Lymphocytes in Inflammatory Arthritis.Frontiers in immunology · 2020Review
- Pain Mechanism in Rheumatoid Arthritis: From Cytokines to Central Sensitization.Mediators of inflammation · 2020Review
- Clinical-like cryotherapy improves footprint patterns and reduces synovial inflammation in a rat model of post-traumatic knee osteoarthritis.Scientific reports · 2019Article
- Knee osteoarthritis induces atrophy and neuromuscular junction remodeling in the quadriceps and tibialis anterior muscles of rats.Scientific reports · 2019Article
- Divergent roles of immune cells and their mediators in pain.Rheumatology (Oxford, England) · 2018Review
- Neutrophil Function in an Inflammatory Milieu of Rheumatoid Arthritis.Journal of immunology research · 2018Review
- IL‑22 expression is increased variedly in the initial phase, onset and chronic phase of a pristane‑induced arthritis rat model.Molecular medicine reports · 2017Article
- Lapachol, a compound targeting pyrimidine metabolism, ameliorates experimental autoimmune arthritis.Arthritis research & therapy · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionRheumatoid arthritis (RA) is a chronic autoimmune disease characterized by neutrophil articular infiltration, joint pain and the progressive destruction of cartilage and bone. IL-22 is a key effector molecule that plays a critical role in autoimmune diseases. However, the function of IL-22 in the pathogenesis of RA remains controversial. In this study, we investigated the role of IL-22 in the early phase of antigen-induced arthritis (AIA) in mice.
methodsAIA was induced in C57BL/6, IL-22(-/-), ASC(-/-) and IL-1R1(-/-) immunized mice challenged intra-articularly with methylated bovine serum albumin (mBSA). Expression of IL-22 in synovial membranes was determined by RT-PCR. Articular hypernociception was evaluated using an electronic von Frey. Neutrophil recruitment and histopathological analyses were assessed in inflamed knee joint. Joint levels of inflammatory mediators and mBSA-specific IgG concentration in the serum were measured by ELISA.
resultsThe IL-22 mRNA expression and protein levels in synovial tissue were increased during the onset of AIA. In addition, pharmacological inhibition (anti-IL-22 antibody) and genetic deficiency (IL-22(-/-) mice) reduced articular pain and neutrophil migration in arthritic mice. Consistent with these findings, recombinant IL-22 joint administration promoted articular inflammation per se in WT mice, restoring joint nociception and neutrophil infiltration in IL-22(-/-) mice. Moreover, IL-22-deficient mice showed reduced synovitis (inflammatory cell influx) and lower joint IL-1β levels, whereas the production of IL-17, MCP-1/CCL2, and KC/CXCL1 and the humoral immune response were similar, compared with WT mice. Corroborating these results, the exogenous administration of IL-22 into the joints induced IL-1β production in WT mice and reestablished IL-1β production in IL-22(-/-) mice challenged with mBSA. Additionally, IL-1R1(-/-) mice showed attenuated inflammatory features induced by mBSA or IL-22 challenge. Articular nociception and neutrophil migration induced by IL-22 were also reduced in ASC(-/-) mice.
conclusionsThese results suggest that IL-22 plays a pro-inflammatory/pathogenic role in the onset of AIA through an ASC-dependent stimulation of IL-1β production.
Indexed as
Identifiers
What OpenQuestion holds
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.