Evidence map›Paper›PMID 29295985›Full record

ArticleNature communications2018

TNF blockade induces a dysregulated type I interferon response without autoimmunity in paradoxical psoriasis.

Curdin Conrad, Jeremy Di Domizio, Alessio Mylonas, Cyrine Belkhodja, Olivier Demaria, Alexander A Navarini, Anne-Karine Lapointe, Lars E French, Maxime Vernez, Michel Gilliet

Registry-linked trialAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03629379 (Response to Ustekinumab for Anti-tnf Induced Psoriasiform Skin Lesions), which is not on this map. Cited by 130 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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.

NCT03629379 phase4completednot on this mapstarted 2019, after this paper: background citation

Response to Ustekinumab for Anti-tnf Induced Psoriasiform Skin Lesions

TypeinterventionalSponsorUniversitaire Ziekenhuizen KU LeuvenRan2019 to 2021Enrolled20ConditionsInflammatory Bowel Diseases, PsoriasisArmsUstekinumab, Vedolizumab
3 · Its place in the literature

Who cites it

130 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Biologic-Induced Paradoxical Psoriatic Alopecia: A Systematic Review.The Australasian journal of dermatology · 2025
    Pooled it
  3. Pooled it
  4. Review
  5. Immune shifts in inflammatory skin diseases.JID innovations : skin science from molecules to population health · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Current landscape of drug induced retinal vasculitis.Journal of ophthalmic inflammation and infection · 2026
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Palmoplantar pustulosis: pathogenesis, differential diagnosis, and treatment.Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG · 2026
    Review
  16. Article
  17. Dermatology 2.0: Precision medicine for inflammatory skin diseases.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026
    Review
  18. Article
  19. Article
  20. Article

70 more citing papers are in PubMed but not listed here.

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

10 authors.

Curdin ConradDepartment of Dermatology, University Hospital CHUV, Lausanne, 1011, Switzerland. curdin.conrad@chuv.ch.
Jeremy Di DomizioDepartment of Dermatology, University Hospital CHUV, Lausanne, 1011, Switzerland.ORCID http://orcid.org/0000-0002-6281-3918
Alessio MylonasDepartment of Dermatology, University Hospital CHUV, Lausanne, 1011, Switzerland.
Cyrine BelkhodjaDepartment of Dermatology, University Hospital CHUV, Lausanne, 1011, Switzerland.
Olivier DemariaDepartment of Dermatology, University Hospital CHUV, Lausanne, 1011, Switzerland.
Alexander A NavariniDepartment of Dermatology, University Hospital of Zurich, Zurich, 8091, Switzerland.
Anne-Karine LapointeDepartment of Dermatology, University Hospital CHUV, Lausanne, 1011, Switzerland.
Lars E FrenchDepartment of Dermatology, University Hospital of Zurich, Zurich, 8091, Switzerland.
Maxime VernezDepartment of Dermatology, University Hospital CHUV, Lausanne, 1011, Switzerland.
Michel GillietDepartment of Dermatology, University Hospital CHUV, Lausanne, 1011, Switzerland. michel.gilliet@chuv.ch.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although anti-tumor necrosis factor (TNF) agents are highly effective in the treatment of psoriasis, 2-5% of treated patients develop psoriasis-like skin lesions called paradoxical psoriasis. The pathogenesis of this side effect and its distinction from classical psoriasis remain unknown. Here we show that skin lesions from patients with paradoxical psoriasis are characterized by a selective overexpression of type I interferons, dermal accumulation of plasmacytoid dendritic cells (pDC), and reduced T-cell numbers, when compared to classical psoriasis. Anti-TNF treatment prolongs type I interferon production by pDCs through inhibition of their maturation. The resulting type I interferon overexpression is responsible for the skin phenotype of paradoxical psoriasis, which, unlike classical psoriasis, is independent of T cells. These findings indicate that paradoxical psoriasis represents an ongoing overactive innate inflammatory process, driven by pDC-derived type I interferon that does not lead to T-cell autoimmunity.

Indexed as

AdalimumabAdolescentAdultAgedAnimalsAntibodies, MonoclonalAutoimmunityCells, CulturedCrohn DiseaseCytokinesDendritic CellsFemaleHumansInfliximabInterferon Type IMaleAdalimumabAntibodies, MonoclonalCytokinesInfliximabInterferon Type ITumor Necrosis Factor-alpha

Identifiers

PMID29295985
PMCPMC5750213

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Registered trials

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.