ArticlePloS one2019
Transition from metal-DTH resistance to susceptibility is facilitated by NLRP3 inflammasome signaling induced Th17 reactivity: Implications for orthopedic implants.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- No difference in patient reported outcome and inflammatory response after coated and uncoated total knee arthroplasty - a randomized controlled study.BMC musculoskeletal disorders · 2023Trial
- Establishing clinically meaningful ranges of metal hypersensitivity in orthopaedic patients using COVID-19 vaccine-induced adaptive immune responses from fully vaccinated adults.Journal of orthopaedics · 2024Article
- Immune response differences in degradable and non-degradable alloy implants.Bioactive materials · 2023Review
- A comprehensive summary of disease variants implicated in metal allergy.Journal of toxicology and environmental health. Part B, Critical reviews · 2022Review
- IL-17A-Mediated Immune-Inflammatory Periarticular Mass and Osteolysis From Impingement in Ceramic-On-Ceramic Total Hip Arthroplasty.Arthroplasty today · 2021Article
- Dental metal hypersensitivity in patients with psoriasis vulgaris: A case-control study using anHealth science reports · 2021Article
- Metal-induced delayed type hypersensitivity responses potentiate particle induced osteolysis in a sex and age dependent manner.PloS one · 2021Article
- What Surgeons Need to Know About Adverse Local Tissue Reaction in Total Hip Arthroplasty.The Journal of arthroplasty · 2020Review
- Do Battlefield Injury-acquired Indwelling Metal Fragments Induce Metal Immunogenicity?Clinical orthopaedics and related research · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Metal hypersensitivity has been recognized as an adverse biologic reaction that can compromise total joint arthroplasty (TJA) performance. However, the etiology of metal hypersensitivity responses in TJAs remains unclear. Metal implant debris is known to act as a danger signal that drives NLRP3 inflammasome activation. It remains unknown if implant debris induced inflammasome activation regulates T cell lineage in TJA metal hypersensitivity responses. In this study, we show both in vivo and in vitro that the pathogenesis of metal hypersensitivity responses to implant debris are largely dependent on activation of the inflammasome/caspase-1 pathway and subsequent production of IL-17A/F by CD4+ T cells. Inhibiting either the inflammasome pathway or IL-17A bioactivity in vivo and in vitro (in vivo using NLRP3 and Caspase-1 deficient mice or in vitro using blocking agents such as Capase-1 inhibitor, IL-1Ra and anti-IL-17A), significantly (p<0.05) mitigated metal-DTH paw inflammation as well as lymphocyte cytokine (IFN-γ and IL-17) and proliferation responses in metal-sensitized mice and primary human PBMCs. This study provides mechanistic insight into how in vivo exposure to orthopedic implant debris, and metals in general, elicits NLRP3 inflammasome activation that mediates the generation of IL-17A/F producing CD4+ T cells, leading to metal-delayed type hypersensitivity reactions.
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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.