ReviewPharmaceutics2020
NLRP3 Inflammasome and Allergic Contact Dermatitis: A Connection to Demystify.
Review in Pharmaceutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 29 citations in OpenAlex.
- A phase 2a double-blind, placebo-controlled, randomized clinical trial evaluating the efficacy and safety of NuGel, a novel topical GPCR19-mediated inflammasome inhibitor, in patients with mild to moderate atopic dermatitis: a proof-of-concept study withFrontiers in immunology · 2025Trial
- Therapeutic targeting of lysosome-triggered inflammatory channels in nasal and upper-airway allergic conditions.Frontiers in immunology · 2026Review
- Allergenic and cytotoxic potential of (meth)acrylate monomers in dental materials: a narrative review.Frontiers in dental medicine · 2026Review
- Immunopathogenesis and immunoregulatory mechanisms in allergic contact dermatitis.Frontiers in immunology · 2026Review
- Review
- Article
- Mesenchymal stem cell-derived extracellular vesicles: a regulator and carrier for targeting bone-related diseases.Cell death discovery · 2024Review
- NLRP3 deficiency aggravated DNFB-induced chronic itch by enhancing type 2 immunity IL-4/TSLP-TRPA1 axis in mice.Frontiers in immunology · 2024Article
- Role of Innate Immunity in Allergic Contact Dermatitis: An Update.International journal of molecular sciences · 2023Review
- Diseases from the Spectrum of Dermatitis and Eczema: Can "Omics" Sciences Help with Better Systematics and More Accurate Differential Diagnosis?International journal of molecular sciences · 2023Review
- A Hydrophilic Sulfated Resveratrol Derivative for Topical Application: Sensitization and Anti-Allergic Potential.Molecules (Basel, Switzerland) · 2023Article
- Emerging role of mesenchymal stem/stromal cells (MSCs) and MSCs-derived exosomes in bone- and joint-associated musculoskeletal disorders: a new frontier.European journal of medical research · 2023Review
- Chemical- and Drug-Induced Allergic, Inflammatory, and Autoimmune Diseases Via Haptenation.Biology · 2023Review
- Role of nuclear receptor PXR in immune cells and inflammatory diseases.Frontiers in immunology · 2022Review
- Mast Cells in the Skin: Defenders of Integrity or Offenders in Inflammation?International journal of molecular sciences · 2021Review
- Non-Coding RNAs: Master Regulators of Inflammasomes in Inflammatory Diseases.Journal of inflammation research · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allergic contact dermatitis is a common occupational disease that manifests as a cell-mediated hypersensitivity reaction following skin exposure to small reactive chemicals termed haptens. Haptens penetrate the stratum corneum and covalently modify proteins in the epidermis, inducing intracellular stress, which further leads to the release of damage-associated molecular patterns (DAMPs), such as uric acid, reactive oxygen species, hyaluronic acid fragments and extracellular adenosine triphosphate (ATP). These DAMPs are recognized by pattern recognition receptors (PRRs) in innate immune cells, namely dendritic cells (DCs), leading to their maturation and migration to the draining lymph nodes where they activate naïve T lymphocytes. Among all PRRs, several studies emphasize the role of NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome on the allergic contact dermatitis (ACD) sensitization phase. However, skin allergens-danger signals-NLRP3 inflammasome axis is yet to be completely elucidated. Therefore, in this review, we sought to discuss the molecular mechanisms underlying DAMPs release and NLRP3 inflammasome activation triggered by skin allergens. The elucidation of these key events might help to identify novel therapeutic strategies for ACD, as well as the development of nonanimal alternative methods for the identification and potency categorization of skin sensitizers.
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.