Evidence map›Paper›PMID 36996217›Full record

ArticleScience (New York, N.Y.)2023

Cytosolic antibody receptor TRIM21 is required for effective tau immunotherapy in mouse models.

Aamir S Mukadam, Lauren V C Miller, Annabel E Smith, Marina Vaysburd, Siri A Sakya, Sophie Sanford, Sophie Keeling, Benjamin J Tuck, Taxiarchis Katsinelos, Chris Green and 14 more

Open access · greenAbstract read
In one paragraph

Article in Science (New York, N.Y.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
9.5field-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

50 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Tripartite motif containing 21 autoimmunity primes CD8Arthritis research & therapy · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. TRIM21 is a molecular rheostat for influenza A virus replication.bioRxiv : the preprint server for biology · 2026
    Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

24 authors at 3 institutions in 2 countries.

Aamir S MukadamUK Dementia Research Institute at the University of Cambridge, Cambridge CB2 0AH, UK.ORCID 0000-0002-3363-7636
Lauren V C Miller *UK Dementia Research Institute at the University of Cambridge, Cambridge CB2 0AH, UK.ORCID 0000-0002-0612-494X
Annabel E Smith *UK Dementia Research Institute at the University of Cambridge, Cambridge CB2 0AH, UK.ORCID 0000-0001-5837-6121
Marina VaysburdMRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.
Siri A SakyaDepartment of Immunology, University of Oslo and Oslo University Hospital Rikshospitalet, N-0424 Oslo, Norway.ORCID 0000-0002-5893-6771
Sophie SanfordUK Dementia Research Institute at the University of Cambridge, Cambridge CB2 0AH, UK.ORCID 0000-0002-7712-0575
Sophie KeelingUK Dementia Research Institute at the University of Cambridge, Cambridge CB2 0AH, UK.ORCID 0000-0002-6413-2550
Benjamin J TuckUK Dementia Research Institute at the University of Cambridge, Cambridge CB2 0AH, UK.ORCID 0000-0002-8148-542X
Taxiarchis KatsinelosUK Dementia Research Institute at the University of Cambridge, Cambridge CB2 0AH, UK.ORCID 0000-0001-6951-3216
Chris GreenUK Dementia Research Institute at the University of Cambridge, Cambridge CB2 0AH, UK.ORCID 0000-0002-4690-7594
Lise SkovUK Dementia Research Institute at the University of Cambridge, Cambridge CB2 0AH, UK.ORCID 0000-0002-7142-7728
Sanne S KaalundDepartment of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0AH, UK.ORCID 0000-0002-8975-1825
Stian FossDepartment of Immunology, University of Oslo and Oslo University Hospital Rikshospitalet, N-0424 Oslo, Norway.ORCID 0000-0001-6527-051X
Keith MayesMRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.
Kevin O'ConnellMRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.
Mark WingMRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.
Claire KnoxMRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.
Jessica BanburyMRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.
Edward AvezovUK Dementia Research Institute at the University of Cambridge, Cambridge CB2 0AH, UK.ORCID 0000-0002-2894-0585
James B RoweDepartment of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0AH, UK.ORCID 0000-0001-7216-8679
Michel GoedertMRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.ORCID 0000-0002-5214-7886
Jan Terje AndersenDepartment of Immunology, University of Oslo and Oslo University Hospital Rikshospitalet, N-0424 Oslo, Norway.ORCID 0000-0003-1710-1628
Leo C JamesMRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.ORCID 0000-0003-2131-0334
William A McEwanUK Dementia Research Institute at the University of Cambridge, Cambridge CB2 0AH, UK.ORCID 0000-0002-4408-0407
University of Cambridge · GBMRC Laboratory of Molecular Biology · GBOslo University Hospital · NO

Funding

Medical Research Council MC_U105181010Medical Research Council MC_U105184291Wellcome Trust 206248
6 · The paper itself

Abstract

Aggregates of the protein tau are proposed to drive pathogenesis in neurodegenerative diseases. Tau can be targeted by using passively transferred antibodies (Abs), but the mechanisms of Ab protection are incompletely understood. In this work, we used a variety of cell and animal model systems and showed that the cytosolic Ab receptor and E3 ligase TRIM21 (T21) could play a role in Ab protection against tau pathology. Tau-Ab complexes were internalized to the cytosol of neurons, which enabled T21 engagement and protection against seeded aggregation. Ab-mediated protection against tau pathology was lost in mice that lacked T21. Thus, the cytosolic compartment provides a site of immunotherapeutic protection, which may help in the design of Ab-based therapies in neurodegenerative disease.

Indexed as

Antibodies, MonoclonalImmunization, PassiveRibonucleoproteinsTauopathiestau ProteinsTripartite Motif ProteinsUbiquitin-Protein LigasesAnimalsCytosolDisease Models, AnimalMiceReceptors, FcSS-A AntigenAntibodies, MonoclonalReceptors, FcRibonucleoproteinsSS-A Antigentau ProteinsTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID36996217
PMCPMC7614512
OpenAlexW4362506504

What OpenQuestion holds

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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.