Evidence map›Paper›PMID 38451381›Full record

ReviewJournal of clinical immunology2024

The Complexity of Being A20: From Biological Functions to Genetic Associations.

Urekha Karri, Magdalena Harasimowicz, Manuel Carpio Tumba, Daniella M Schwartz

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of clinical immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
10.8field-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

34 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. How I Treat: Haploinsufficiency of A20.Journal of human immunity · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Monogenic disorders of the TNF signalling pathway.Nature reviews. Rheumatology · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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 1 institution in 1 country.

Urekha Karri *Departments of Medicine and Immunology, Division of Rheumatology and Clinical Immunology, University of Pittsburgh, 200 Lothrop St., Pittsburgh, PA, 15213, USA.
Magdalena Harasimowicz *Departments of Medicine and Immunology, Division of Rheumatology and Clinical Immunology, University of Pittsburgh, 200 Lothrop St., Pittsburgh, PA, 15213, USA.
Manuel Carpio TumbaDepartments of Medicine and Immunology, Division of Rheumatology and Clinical Immunology, University of Pittsburgh, 200 Lothrop St., Pittsburgh, PA, 15213, USA.
Daniella M SchwartzDepartments of Medicine and Immunology, Division of Rheumatology and Clinical Immunology, University of Pittsburgh, 200 Lothrop St., Pittsburgh, PA, 15213, USA. Daniella.Schwartz@pitt.edu.
University of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A20, encoded by TNFAIP3, is a critical negative regulator of immune activation. A20 is a ubiquitin editing enzyme with multiple domains, each of which mediates or stabilizes a key ubiquitin modification. A20 targets diverse proteins that are involved in pleiotropic immunologic pathways. The complexity of A20-mediated immunomodulation is illustrated by the varied effects of A20 deletion in different cell types and disease models. Clinically, the importance of A20 is highlighted by its extensive associations with human disease. A20 germline variants are associated with a wide range of inflammatory diseases, while somatic mutations promote development of B cell lymphomas. More recently, the discovery of A20 haploinsufficiency (HA20) has provided real world evidence for the role of A20 in immune cell function. Originally described as an autosomal dominant form of Behcet's disease, HA20 is now considered a complex inborn error of immunity with a broad spectrum of immunologic and clinical phenotypes.

Indexed as

Behcet SyndromeTumor Necrosis Factor alpha-Induced Protein 3Germ-Line MutationHaploinsufficiencyHumansImmunomodulationUbiquitinsTNFAIP3 protein, humanTumor Necrosis Factor alpha-Induced Protein 3UbiquitinsA20A20 haploinsufficiencyautoinflammatory diseaseimmune dysregulation diseaseinborn error of immunityreviewTNFAIP3TNFAIP3 gene mutationubiquitin

Identifiers

PMID38451381
OpenAlexW4392563565

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.