Evidence map›Paper›PMID 37071038›Full record

ArticleImmunoHorizons2023

Guselkumab More Effectively Neutralizes Psoriasis-Associated Histologic, Transcriptomic, and Clinical Measures than Ustekinumab.

Kim Campbell, Katherine Li, Feifei Yang, Patrick Branigan, M Merle Elloso, Jacqueline Benson, Yevgeniya Orlovsky, Yanqing Chen, Sandra Garcet, James G Krueger

Open access · goldAbstract read
In one paragraph

Article in ImmunoHorizons, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 13 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Unveiling Psoriasis: Delving into Pathogenesis, Treatment Breakthroughs, and Patent Trends.Recent advances in inflammation & allergy drug discovery · 2025
    Review
  11. Article
  12. Review
  13. The Role of Epigenetic Factors in the Pathogenesis of Psoriasis.International journal of molecular sciences · 2024
    Review
  14. Review
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 at 2 institutions in 1 country.

Kim CampbellJanssen Research & Development, LLC, Spring House, PA.ORCID 0000-0003-3789-416X
Katherine LiJanssen Research & Development, LLC, Spring House, PA.
Feifei YangJanssen Research & Development, LLC, Spring House, PA.
Patrick BraniganJanssen Research & Development, LLC, Spring House, PA.ORCID 0000-0001-9741-9067
M Merle EllosoJanssen Scientific Affairs, LLC, Horsham, PA.
Jacqueline BensonJanssen Research & Development, LLC, Spring House, PA.
Yevgeniya OrlovskyJanssen Research & Development, LLC, Spring House, PA.
Yanqing ChenJanssen Research & Development, LLC, Spring House, PA.ORCID 0000-0002-9534-6199
Sandra GarcetThe Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY.
James G KruegerThe Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY.
Janssen (United States) · USRockefeller University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Given the key role of the IL-23/Th17 axis in the pathogenesis of moderate-to-severe plaque psoriasis, several specific inhibitors of the p19 subunit of IL-23 have been approved to treat this chronic inflammatory disease. Clinical data indicate that guselkumab, one such selective IL-23 inhibitor, achieves greater clinical efficacy compared with ustekinumab, which inhibits both IL-12 and IL-23 via binding their shared p40 subunit. To understand mechanisms underlying the enhanced efficacy observed with the p19 subunit of IL-23-specific inhibition, we explored cellular and molecular changes in skin of psoriasis patients treated with ustekinumab or guselkumab and in ustekinumab inadequate responders (Investigator's Global Assessment of psoriasis score ≥ 2) subsequently treated with guselkumab (ustekinumab→guselkumab). Skin biopsies were collected pretreatment and posttreatment to assess histologic changes and molecular responses in ustekinumab- and guselkumab-treated patients. Serum cytokines and skin transcriptomics from the subset of ustekinumab→guselkumab-treated patients were also analyzed to characterize differential treatment effects. Ustekinumab and guselkumab demonstrated differential effects on secretion of pathogenic Th17-related cytokines induced by IL-23 in in vitro assays, which suggest guselkumab is a more potent therapeutic agent. Consistent with these findings, guselkumab elicited a significantly greater reduction in cellular and molecular psoriasis-related disease indicators than ustekinumab. In ustekinumab→guselkumab patients, suppression of serum IL-17A and IL-17F levels and neutralization of molecular scar and psoriasis-related gene markers in skin were significantly greater compared with patients continuing ustekinumab. This comparative study demonstrates that guselkumab inhibits psoriasis-associated pathology, suppresses Th17-related serum cytokines, and normalizes the psoriasis skin gene expression profile more effectively than ustekinumab.

Indexed as

PsoriasisUstekinumabAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedCytokinesHumansInterleukin-23TranscriptomeAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedCytokinesguselkumabInterleukin-23Ustekinumab

Identifiers

PMID37071038
PMCPMC10579843
OpenAlexW4366236768

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.