Evidence map›Paper›PMID 29875316›Full record

ArticleJCI insight2018

CD83 expression is essential for Treg cell differentiation and stability.

Marina Doebbeler, Christina Koenig, Lena Krzyzak, Christine Seitz, Andreas Wild, Thomas Ulas, Kevin Baßler, Dmitry Kopelyanskiy, Alina Butterhof, Christine Kuhnt and 13 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

39 citing papers in PubMed, 56 citations in OpenAlex.

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  8. γδ T cells: The first line of defense for neonates.The Journal of experimental medicine · 2024
    Article
  9. Article
  10. IL-23 stabilizes an effector TNature immunology · 2024
    Article
  11. Article
  12. Article
  13. CD83 Regulates the Immune Responses in Inflammatory Disorders.International journal of molecular sciences · 2023
    Review
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  15. Article
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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

23 authors at 4 institutions in 1 country.

Marina DoebbelerDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
Christina KoenigDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
Lena KrzyzakDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
Christine SeitzDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
Andreas WildDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
Thomas UlasGenomics & Immunoregulation, LIMES-Institute, University of Bonn, Bonn, Germany.
Kevin BaßlerGenomics & Immunoregulation, LIMES-Institute, University of Bonn, Bonn, Germany.
Dmitry KopelyanskiyGenomics & Immunoregulation, LIMES-Institute, University of Bonn, Bonn, Germany.
Alina ButterhofDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
Christine KuhntDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
Simon KreiserDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
Lena StichDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
Elisabeth ZinserDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
Ilka KnippertzDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
Stefan WirtzDepartment of Medicine 1, University Hospital Erlangen, Erlangen, Germany.
Christin RiegelDepartment of Internal Medicine 3, University Hospital Regensburg, Regensburg, Germany.
Petra HoffmannDepartment of Internal Medicine 3, University Hospital Regensburg, Regensburg, Germany.
Matthias EdingerDepartment of Internal Medicine 3, University Hospital Regensburg, Regensburg, Germany.
Lars NitschkeDivision of Genetics, Department of Biology, University of Erlangen-Nürnberg, Erlangen, Germany.
Thomas WinklerDivision of Genetics, Department of Biology, University of Erlangen-Nürnberg, Erlangen, Germany.
Joachim L SchultzeGenomics & Immunoregulation, LIMES-Institute, University of Bonn, Bonn, Germany.
Alexander SteinkassererDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
Matthias LechmannDepartment of Immune Modulation at the Department of Dermatology, University Hospital Erlangen, Erlangen, Germany.
Universitätsklinikum Erlangen · DEUniversity of Bonn · DEUniversity Hospital Regensburg · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Foxp3-positive regulatory T cells (Tregs) are crucial for the maintenance of immune homeostasis and keep immune responses in check. Upon activation, Tregs are transferred into an effector state expressing transcripts essential for their suppressive activity, migration, and survival. However, it is not completely understood how different intrinsic and environmental factors control differentiation. Here, we present for the first time to our knowledge data suggesting that Treg-intrinsic expression of CD83 is essential for Treg differentiation upon activation. Interestingly, mice with Treg-intrinsic CD83 deficiency are characterized by a proinflammatory phenotype. Furthermore, the loss of CD83 expression by Tregs leads to the downregulation of Treg-specific differentiation markers and the induction of an inflammatory profile. In addition, Treg-specific conditional knockout mice showed aggravated autoimmunity and an impaired resolution of inflammation. Altogether, our results show that CD83 expression in Tregs is an essential factor for the development and function of effector Tregs upon activation. Since Tregs play a crucial role in the maintenance of immune tolerance and thus prevention of autoimmune disorders, our findings are also clinically relevant.

Indexed as

AutoimmunityAnimalsAntigens, CDCD83 AntigenCell DifferentiationFemaleImmune ToleranceImmunoglobulinsLymphocyte ActivationMaleMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutModels, AnimalT-Lymphocytes, RegulatoryAntigens, CDCD83 AntigenImmunoglobulinsMembrane GlycoproteinsAutoimmune diseasesAutoimmunityImmunologyT cell developmentTolerance

Identifiers

PMID29875316
PMCPMC6124443
OpenAlexW2806989348

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.