ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
From acute mast cell activation to a structured immunothrombotic and autoimmune niche in chronic spontaneous urticaria.
Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic spontaneous urticaria (CSU) presents recurrent wheals and/or angioedema for more than six weeks without an identifiable trigger. Although mast cell activation and histamine release are well-established effector mechanisms, this model does not explain disease persistence, immune dysregulation, or treatment refractoriness. A deeper mechanistic framework is required to explain progression to chronic disease. PURPOSE: To propose a stage-wise CSU chronification model, reframing the disease as a structured dermal immunothrombotic and autoimmune niche rather than an episodic mast cell-effector event, and to derive therapeutic implications.
methodsA narrative synthesis of ultrastructural, immunohistochemical, transcriptomic, and clinical evidence from the published clinical literature, including original studies from our group on acute drug-induced urticaria and antihistamine-refractory CSU was performed.
resultsFive sequential stages drive chronification: (1) FcεRI/BTK-dependent mast cell degranulation; (2) eosinophil tissue-factor activation of the coagulation-complement loop; (3) FXIIIa⁺ dendrocyte phagocytosis and T-cell priming via OX40/OX40L; (4) Th2-driven M2 macrophage polarization with autoantibody-mediated mast cell reactivation; and (5) JAK/STAT and IFN-λ1 signaling sustaining dermal immune niche. Transcriptomic hub genes and cytokine profiling further support this model.
conclusionCSU reflects a structured immune architecture rather than isolated mast cell activation. This explains treatment refractoriness and supports targeting upstream checkpoints, including BTK, JAK, and OX40/OX40L for sustained control.
Indexed as
Identifiers
42393364What Socratic 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 Socratic graph.