ReviewExperimental and therapeutic medicine2022
Immunological signature of chronic spontaneous urticaria (Review).
Review in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Autohemotherapy combined with other external treatments of Traditional Chinese Medicine for chronic urticaria: a systematic review and meta-analysis.Frontiers in medicine · 2026Pooled it
- Pharmacology and safety of TAS5315, a Bruton tyrosine kinase inhibitor, in healthy volunteers: First-in-human, randomized, ascending-dose studies.British journal of clinical pharmacology · 2025Trial
- Article
- Evaluation of Vitamin B12 Levels in Chronic Spontaneous Urticaria Patients and Correlation with Severity of Disease.Maedica · 2026Article
- Chronic spontaneous cholinergic urticaria: advances in immunological mechanisms focusing on neuro-immune crosstalk and novel targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Type 2 Inflammation and Its Role in Dermatologic Diseases.International journal of dermatology · 2025Review
- Exploring the Impact of IL-33 Gene Polymorphism (International journal of molecular sciences · 2024Article
- Alarmins in Chronic Spontaneous Urticaria: Immunological Insights and Therapeutic Perspectives.Biomedicines · 2024Review
- Changes in Serum IL-12 Levels following the Administration of H1-Antihistamines in Patients with Chronic Spontaneous Urticaria.Journal of personalized medicine · 2024Article
- The Alarmin Triad-IL-25, IL-33, and TSLP-Serum Levels and Their Clinical Implications in Chronic Spontaneous Urticaria.International journal of molecular sciences · 2024Article
- Levels of serum inflammatory cytokines and their correlations with disease severity in patients with chronic spontaneous urticaria.Postepy dermatologii i alergologii · 2024Article
- Evaluation of the Immune Checkpoints, TIM-3 and PD-1, as well as Anti-Inflammatory Cytokines IL-10, and TGF-β along with Diseases Activity in Chronic Spontaneous Urticaria.International journal of molecular and cellular medicine · 2024Article
- Omalizumab for Patients with Chronic Spontaneous Urticaria: A Narrative Review of Current Status.Dermatology and therapy · 2023Review
- Intradermal substance P as a challenge agent in healthy individuals.Clinical and translational science · 2023Article
- IL-31-Pruritus Interleukin: Serum Values and Clinical Impact in Chronic Spontaneous Urticaria-A Romanian Retrospective Study.Journal of clinical medicine · 2023Article
- Treatment of Urticaria caused by severe cryptosporidiosis in a 17-month-old child - a case report.BMC infectious diseases · 2023Article
- The correlation between Th17/Treg immune dysregulation and the disease severity in chronic spontaneous urticaria patients.Immunity, inflammation and disease · 2023Article
- Functional connectivity impairment of thalamus-cerebellum-scratching neural circuits in pruritus of chronic spontaneous urticaria.Frontiers in neuroscience · 2022Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic urticaria (CU) is a condition characterized by intensely pruritic, edematous, erythematous papules lasting for more than 6 weeks. Over half of the cases have concomitant swelling of deeper tissues, known as angioedema. The socio-economic burden of the disease is significant. Unfortunately, patients with severe CU, refractory to conventional treatment, have limited and expensive therapeutic options. The pathogenesis of CU is not yet completely understood. Therefore, elucidating the pathophysiological mechanisms involved would potentially identify new therapeutic targets. It has been accepted in recent years that mast cells and their activation, followed by excessive degranulation represent the key pathophysiological events in chronic spontaneous urticaria (CSU). The triggering events and the complexity of the effector mechanisms, however, remain intensely debated topics with conflicting studies. One pathogenetic mechanism incriminated in chronic spontaneous urticaria is the response mediated by the high-affinity receptor for IgE (FcεRI) expressed on mast cells. Increasing recognition of chronic spontaneous urticaria as an autoimmune disease linked to the cytokine-chemokine network imbalance resulting from alteration of innate immune response is another pathogenetic explanation. It is likely that these different pathological mechanisms are more interconnected, both acting synergistically, rather than separately, to produce the clinical expression of CU. The discovery and understanding of pathogenic mechanisms represent the premise for the development of safe and effective immunomodulators and targeted biological treatment for severe, refractory CU.
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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 Socratic graph.