Evidence map›Paper›PMID 33824526›Full record

ReviewNature reviews. Rheumatology2021

Immunological memory in rheumatic inflammation - a roadblock to tolerance induction.

Patrick Maschmeyer, Hyun-Dong Chang, Qingyu Cheng, Mir-Farzin Mashreghi, Falk Hiepe, Tobias Alexander, Andreas Radbruch

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
2.3field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 38 citations in OpenAlex.

  1. Guideline
  2. Guideline
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  4. Review
  5. Article
  6. Sequential immunotherapy: towards cures for autoimmunity.Nature reviews. Drug discovery · 2024
    Review
  7. New dawn of cellular therapies in autoimmune diseases.Molecular therapy. Methods & clinical development · 2023
    Article
  8. Article
  9. Innate immune memory in inflammatory arthritis.Nature reviews. Rheumatology · 2023
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
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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

7 authors at 2 institutions in 1 country.

Patrick Maschmeyer *Deutsches Rheuma-Forschungszentrum Berlin, a Leibniz Institute, Berlin, Germany.
Hyun-Dong Chang *Deutsches Rheuma-Forschungszentrum Berlin, a Leibniz Institute, Berlin, Germany.ORCID http://orcid.org/0000-0002-7341-4533
Qingyu ChengDepartment of Rheumatology and Clinical Immunology, Charité Universitätsmedizin Berlin, Berlin, Germany.
Mir-Farzin MashreghiDeutsches Rheuma-Forschungszentrum Berlin, a Leibniz Institute, Berlin, Germany.ORCID http://orcid.org/0000-0002-8015-6907
Falk HiepeDepartment of Rheumatology and Clinical Immunology, Charité Universitätsmedizin Berlin, Berlin, Germany.
Tobias AlexanderDepartment of Rheumatology and Clinical Immunology, Charité Universitätsmedizin Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0003-1193-0097
Andreas RadbruchDeutsches Rheuma-Forschungszentrum Berlin, a Leibniz Institute, Berlin, Germany. radbruch@drfz.de.ORCID http://orcid.org/0000-0001-5753-0000
German Rheumatism Research Centre · DECharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Why do we still have no cure for chronic inflammatory diseases? One reason could be that current therapies are based on the assumption that chronic inflammation is driven by persistent 'acute' immune reactions. Here we discuss a paradigm shift by suggesting that beyond these reactions, chronic inflammation is driven by imprinted, pathogenic 'memory' cells of the immune system. This rationale is based on the observation that in patients with chronic inflammatory rheumatic diseases refractory to conventional immunosuppressive therapies, therapy-free remission can be achieved by resetting the immune system; that is, by ablating immune cells and regenerating the immune system from stem cells. The success of this approach identifies antigen-experienced and imprinted immune cells as essential and sufficient drivers of inflammation. The 'dark side' of immunological memory primarily involves memory plasma cells secreting pathogenic antibodies and memory T lymphocytes secreting pathogenic cytokines and chemokines, but can also involve cells of innate immunity. New therapeutic strategies should address the persistence of these memory cells. Selective targeting of pathogenic immune memory cells could be based on their specificity, which is challenging, or on their lifestyle, which differs from that of protective immune memory cells, in particular for pathogenic T lymphocytes. The adaptations of such pathogenic memory cells to chronic inflammation offers entirely new therapeutic options for their selective ablation and the regeneration of immunological tolerance.

Indexed as

Immune ToleranceImmunity, InnateAnimalsHumansImmunologic MemoryImmunosuppression TherapyImmunosuppressive AgentsRheumatic DiseasesImmunosuppressive Agents

Identifiers

PMID33824526
OpenAlexW3146742891

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.