ReviewAllergy2023
Protease allergens as initiators-regulators of allergic inflammation.
Review in Allergy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 65 citations in OpenAlex.
- Fungi in Asthma: From Epidemiology and Airway Mycobiome to Molecular Mechanisms and Novel Allergenic Phytopathogens.International journal of molecular sciences · 2026Review
- Common Ragweed Allergy Under Global Change Linking Invasion-Driven Aeroallergen Exposure with Molecular Sensitization and Allergic Airway Disease.Life (Basel, Switzerland) · 2026Review
- Rewiring Atopic Dermatitis: Alarmin Cytokines at the Core of Barrier-Immune-Neuro-Microbiome Networks.Clinical reviews in allergy & immunology · 2026Review
- Classroom microbiome signatures of pest management associate with reduced asthma symptoms.The Journal of allergy and clinical immunology · 2026Article
- Deep Learning-Based Prediction of Epithelial Cytokine Responses for the Selection of Functionally Consistent Airway Organoids.Biomimetics (Basel, Switzerland) · 2026Article
- Epithelial alarmins TSLP, IL-33, and IL-25 in asthma pathogenesis: mechanistic roles and therapeutic implications.Molecular biology reports · 2026Review
- Multiple roads to IgE memory: A pluralistic model of IgE immunity.Cell reports · 2026Review
- Combined Exposure to Ragweed and House Dust Mite Exacerbates Airway Epithelial Barrier Dysfunction: A Multimodal Approach.Medicina (Kaunas, Lithuania) · 2026Article
- Identifying microbial protease allergens through protein language model-guided homology.Cell systems · 2026Article
- Impact of liquid dosing and associated cell 'drowning' in a 3D human bronchial epithelial model used for protease exposure studies.Frontiers in toxicology · 2026Article
- Article
- Catalytic Site Inhibitors of Group 1 Allergens Prevent Toll-like Receptor (TLR)4- and TLR1/2-Dependent Innate Responses in Keratinocytes and Airway Epithelial Cells Exposed to House Dust Mite Allergenic Extract.ACS pharmacology & translational science · 2025Article
- Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic march.Cell reports · 2025Article
- Phenotypic Changes and Oxidative Stress in THP-1 Macrophages in Response to Vanilloids Following Stimulation with Allergen Act d 1 and LPS.Antioxidants (Basel, Switzerland) · 2025Article
- Current Understanding of Epithelial-Derived Alarmins in Chronic Rhinosinusitis with Nasal Polyps.Clinical reviews in allergy & immunology · 2025Review
- Update on HDM Allergy: Principal Changes over the Years.International journal of molecular sciences · 2025Review
- Deficiency of Toll-like receptor 4 attenuates airway inflammation and remodeling in an ovalbumine-induced mouse asthma model.Journal of thoracic disease · 2025Article
- Activation of the Coagulation Cascade as a Universal Danger Sign.Current issues in molecular biology · 2025Review
- How type-2 dendritic cells induce Th2 differentiation: Instruction, repression, or fostering T cell-T cell communication?Allergy · 2025Review
- Nano-Drug Delivery System Targeting the Oxidative Stress Microenvironment: A Prospective Strategy for Intervertebral Disc Degeneration Treatment.International journal of nanomedicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 8 institutions in 5 countries.
Funding
Abstract
Tremendous progress in the last few years has been made to explain how seemingly harmless environmental proteins from different origins can induce potent Th2-biased inflammatory responses. Convergent findings have shown the key roles of allergens displaying proteolytic activity in the initiation and progression of the allergic response. Through their propensity to activate IgE-independent inflammatory pathways, certain allergenic proteases are now considered as initiators for sensitization to themselves and to non-protease allergens. The protease allergens degrade junctional proteins of keratinocytes or airway epithelium to facilitate allergen delivery across the epithelial barrier and their subsequent uptake by antigen-presenting cells. Epithelial injuries mediated by these proteases together with their sensing by protease-activated receptors (PARs) elicit potent inflammatory responses resulting in the release of pro-Th2 cytokines (IL-6, IL-25, IL-1β, TSLP) and danger-associated molecular patterns (DAMPs; IL-33, ATP, uric acid). Recently, protease allergens were shown to cleave the protease sensor domain of IL-33 to produce a super-active form of the alarmin. At the same time, proteolytic cleavage of fibrinogen can trigger TLR4 signaling, and cleavage of various cell surface receptors further shape the Th2 polarization. Remarkably, the sensing of protease allergens by nociceptive neurons can represent a primary step in the development of the allergic response. The goal of this review is to highlight the multiple innate immune mechanisms triggered by protease allergens that converge to initiate the allergic response.
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.