Evidence map›Paper›PMID 26000152›Full record

ReviewAuto- immunity highlights2014

The Th17 axis in psoriatic disease: pathogenetic and therapeutic implications.

Beatrice Marinoni, Angela Ceribelli, Marco S Massarotti, Carlo Selmi

Open access · diamondAbstract readReview
In one paragraph

Review in Auto- immunity highlights, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 104 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Phase 1 study of balinatunfib, an oral inhibitor of TNFR1 signal in mild-to-moderate psoriasis.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026
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  5. A New Method of Canine CD4International journal of molecular sciences · 2025
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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

4 authors at 1 institution in 1 country.

Beatrice MarinoniDivision of Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center, Rozzano, Milan Italy ; Biometra Department, University of Milan, Milan, Italy.
Angela CeribelliDivision of Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center, Rozzano, Milan Italy ; Biometra Department, University of Milan, Milan, Italy.
Marco S MassarottiDivision of Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center, Rozzano, Milan Italy.
Carlo SelmiDivision of Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center, Rozzano, Milan Italy ; Biometra Department, University of Milan, Milan, Italy ; Division of Rheumatology, Allergy and Clinical Immunology, Genome and Biomedical Sciences Facility, University of California at Davis School of Medicine, 451 Health Sciences Drive, Suite 6510, Davis, CA 95616 USA.
Humanitas University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis and psoriatic arthritis represent two paradigmatic conditions characterized by chronic inflammation and possibly autoimmunity, despite the absence of known serum autoantibodies. The two diseases, albeit strongly correlated from clinical, genetic, and epidemiogical standpoints, manifest significant differences in terms of etiology and pathogenetic mechanisms. Nonetheless, Th17 cells appear crucial to both diseases, and IL23 is the cytokine involved in determining the fate of naive CD4+ cells to differentiate into a pathogenic phenotype. This basic experimental observation led to a clear understanding of the immune dysfunction causing psoriasis and psoriatic arthritis but, more importantly, also led to new therapeutic approaches. In recent years, monoclonal antibodies directed to IL12/IL23 (ustekinumab) or IL17 (secukinumab, ixekizumab, brodalumab) are being investigated or have proven to be beneficial for patients with psoriatic disease, thus further supporting the view that Th17 cells play a pivotal role in disease onset and perpetuation. These most recent reports indeed represent significant developments that may allow overcoming the TNFα pathway as the major therapeutic target in chronic inflammation.

Indexed as

IL12IL17IL23InflammationPsoriasisPsoriatic arthritis

Identifiers

PMID26000152
PMCPMC4389010
OpenAlexW1980055161

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.