Evidence map›Paper›PMID 9421487›Full record

ArticleThe Journal of clinical investigation1998

Anti-FcepsilonRIalpha autoantibodies in autoimmune-mediated disorders. Identification of a structure-function relationship.

E Fiebiger, F Hammerschmid, G Stingl, D Maurer

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
10.9field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 254 citations in OpenAlex.

  1. Article
  2. Exploring the Impact of IL-33 Gene Polymorphism (International journal of molecular sciences · 2024
    Article
  3. Article
  4. Chronic Spontaneous Urticaria: Etiology and Pathogenesis.Immunology and allergy clinics of North America · 2024
    Review
  5. Research hotspots in urticaria: A bibliometric study of the top 100 most cited articles.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024
    Article
  6. Research progress in the pathogenesis of chronic urticaria.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Frontiers in medicine · 2022
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Autoimmune Pemphigus: Latest Advances and Emerging Therapies.Frontiers in molecular biosciences · 2021
    Review
  16. Review
  17. Article
  18. Presence of positive skin prick tests to inhalant allergens and markers of T2 inflammation in subjects with chronic spontaneous urticaria (CSU): a systematic literature review.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2020
    Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

E FiebigerDepartment of Dermatology, Division of Immunology, Allergy and Infectious Diseases (DIAID), University of Vienna Medical School, A-1090 Vienna, Austria.
F Hammerschmid
G Stingl
D Maurer
Medical University of Vienna · ATNovartis (Austria) · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-FcepsilonRIalpha autoantibodies (autoAbs) occur and may be of pathogenetic relevance in a subset of chronic urticaria (CU) patients. To analyze the prevalence and magnitude of the humoral anti-FcepsilonRIalpha response in cohorts of CU patients compared with individuals suffering from classic skin- related (auto)immune diseases, we developed an ELISA system for the measurement of anti-FcepsilonRIalpha autoAbs in nonfractionated serum samples. Results obtained using this assay correlated well with those generated by Western blotting. We found IgG anti-FcepsilonRIalpha autoreactivity in 38% of CU patients but not in atopic dermatitis patients, psoriatics, or healthy individuals. We frequently detected anti-FcepsilonRIalpha autoAbs in pemphigus vulgaris (PV, 39%), dermatomyositis (DM, 36%), systemic lupus erythematosus (SLE, 20%), and bullous pemphigoid (BP, 13%). While the autoAb titers in DM, SLE, BP, and PV were similar to those encountered in CU patients, only anti-FcepsilonRIalpha+ CU serum specimens displayed pronounced histamine-releasing activity. The anti-FcepsilonRIalpha autoAbs in CU patients belong predominantly to the complement-fixing subtypes IgG1 and IgG3, whereas in DM, PV, and BP, they were found to be mainly of the IgG2 or IgG4 subtype. Complement-activating properties of anti-FcepsilonRIalpha autoAbs can indeed be of pathogenetic relevance, because C5a receptor blockade on basophils as well as decomplementation reduced drastically the histamine-releasing capacity of most anti-FcepsilonRIalpha-reactive CU sera. As a consequence, therapeutic efforts in CU should aim at altering not only the quantity but also the complement-activating properties of IgG anti-FcepsilonRIalpha autoAbs.

Indexed as

Antigens, CDAutoantibodiesAutoimmune DiseasesBasophilsChronic DiseaseComplement C5aEnzyme-Linked Immunosorbent AssayHistamine ReleaseHumansImmunoglobulin GImmunoglobulin IsotypesReceptor, Anaphylatoxin C5aReceptors, ComplementReceptors, IgERecombinant ProteinsSolubilityAntigens, CDAutoantibodiesComplement C5aImmunoglobulin GImmunoglobulin IsotypesReceptor, Anaphylatoxin C5aReceptors, ComplementReceptors, IgERecombinant Proteins

Identifiers

PMID9421487
PMCPMC508561
OpenAlexW2068972960

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.