Evidence map›Paper›PMID 31324882›Full record

ArticleCellular & molecular immunology2020

Keratinocytes costimulate naive human T cells via CD2: a potential target to prevent the development of proinflammatory Th1 cells in the skin.

Christian Orlik, Daniel Deibel, Johanna Küblbeck, Emre Balta, Sabina Ganskih, Jüri Habicht, Beate Niesler, Jutta Schröder-Braunstein, Knut Schäkel, Guido Wabnitz and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.2field-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

40 citing papers in PubMed, 51 citations in OpenAlex.

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  12. CD2 expressing innate lymphoid and T cells are critical effectors of immunopathogenesis in hidradenitis suppurativa.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. Article
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  15. Article
  16. The Immunology of Psoriasis-Current Concepts in Pathogenesis.Clinical reviews in allergy & immunology · 2024
    Review
  17. Article
  18. Identification of driving genes of familial adenomatous polyposis by differential gene expression analysis and weighted gene co-expression network analysis.Technology and health care : official journal of the European Society for Engineering and Medicine · 2024
    Article
  19. 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

11 authors at 1 institution in 1 country.

Christian OrlikInstitute of Immunology, Section Molecular Immunology, Heidelberg University, Im Neuenheimer Feld 305, 69120, Heidelberg, Germany.
Daniel DeibelInstitute of Immunology, Section Molecular Immunology, Heidelberg University, Im Neuenheimer Feld 305, 69120, Heidelberg, Germany.
Johanna KüblbeckInstitute of Immunology, Section Molecular Immunology, Heidelberg University, Im Neuenheimer Feld 305, 69120, Heidelberg, Germany.
Emre BaltaInstitute of Immunology, Section Molecular Immunology, Heidelberg University, Im Neuenheimer Feld 305, 69120, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-4200-9738
Sabina GanskihInstitute of Immunology, Section Molecular Immunology, Heidelberg University, Im Neuenheimer Feld 305, 69120, Heidelberg, Germany.
Jüri HabichtInstitute of Immunology, Section Molecular Immunology, Heidelberg University, Im Neuenheimer Feld 305, 69120, Heidelberg, Germany.
Beate NieslerInstitute of Human Genetics, Department of Human Molecular Genetics, and nCounter Core Facility, Heidelberg University, Im Neuenheimer Feld 366, 69120, Heidelberg, Germany.
Jutta Schröder-BraunsteinInstitute of Immunology, Section Molecular Immunology, Heidelberg University, Im Neuenheimer Feld 305, 69120, Heidelberg, Germany.
Knut SchäkelDepartment of Dermatology, Heidelberg University, Im Neuenheimer Feld 440, 69120, Heidelberg, Germany.
Guido WabnitzInstitute of Immunology, Section Molecular Immunology, Heidelberg University, Im Neuenheimer Feld 305, 69120, Heidelberg, Germany.
Yvonne SamstagInstitute of Immunology, Section Molecular Immunology, Heidelberg University, Im Neuenheimer Feld 305, 69120, Heidelberg, Germany. yvonne.samstag@urz.uni-heidelberg.de.
Heidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interplay between keratinocytes and immune cells, especially T cells, plays an important role in the pathogenesis of chronic inflammatory skin diseases. During psoriasis, keratinocytes attract T cells by releasing chemokines, while skin-infiltrating self-reactive T cells secrete proinflammatory cytokines, e.g., IFNγ and IL-17A, that cause epidermal hyperplasia. Similarly, in chronic graft-versus-host disease, allogenic IFNγ-producing Th1/Tc1 and IL-17-producing Th17/Tc17 cells are recruited by keratinocyte-derived chemokines and accumulate in the skin. However, whether keratinocytes act as nonprofessional antigen-presenting cells to directly activate naive human T cells in the epidermis remains unknown. Here, we demonstrate that under proinflammatory conditions, primary human keratinocytes indeed activate naive human T cells. This activation required cell contact and costimulatory signaling via CD58/CD2 and CD54/LFA-1. Naive T cells costimulated by keratinocytes selectively differentiated into Th1 and Th17 cells. In particular, keratinocyte-initiated Th1 differentiation was dependent on costimulation through CD58/CD2. The latter molecule initiated STAT1 signaling and IFNγ production in T cells. Costimulation of T cells by keratinocytes resulting in Th1 and Th17 differentiation represents a new explanation for the local enrichment of Th1 and Th17 cells in the skin of patients with a chronic inflammatory skin disease. Consequently, local interference with T cell-keratinocyte interactions may represent a novel strategy for the treatment of Th1 and Th17 cell-driven skin diseases.

Indexed as

CD2 AntigensCD58 AntigensCell DifferentiationCytokinesDendritic CellsEpidermisHumansInflammationIntercellular Adhesion Molecule-1Interferon-gammaKeratinocytesLeukocyte Common AntigensLymphocyte ActivationLymphocyte Function-Associated Antigen-1PhosphorylationProtein BindingCCR7 protein, humanCD2 AntigensCD58 AntigensCytokinesIntercellular Adhesion Molecule-1Interferon-gammaLeukocyte Common AntigensLymphocyte Function-Associated Antigen-1Receptors, CCR7STAT1 Transcription FactorCD2costimulationhuman T cellsinflammatory skin diseaseskeratinocytesLFA-1nonprofessional antigen-presenting cellspsoriasisTh17 cellsTh1 cells

Identifiers

PMID31324882
PMCPMC7109061
OpenAlexW2963590406

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.