Evidence map›Paper›PMID 10225967›Full record

Trial reportThe Journal of clinical investigation1999

CTLA4Ig-mediated blockade of T-cell costimulation in patients with psoriasis vulgaris.

J R Abrams, M G Lebwohl, C A Guzzo, B V Jegasothy, M T Goldfarb, B S Goffe, A Menter, N J Lowe, G Krueger, M J Brown and 9 more

Registry-linked trialOpen access · bronzeAbstract readClinical TrialClinical Trial, Phase IMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Trial report in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00505375 (Effects of CTLA-4 Ig), which is not on this map. Cited by 153 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed, 4 pooled it
14.9field-weighted citation impact, top 1% 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.

NCT00505375 phase2completednot on this mapstarted 2008, after this paper: background citation

Effects of CTLA-4 Ig (Abatacept) On The Progression of Type 1 Diabetes In New Onset Subjects

TypeinterventionalSponsorNational Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)Ran2008 to 2012Enrolled112ConditionsType 1 Diabetes MellitusArmsCTLA-4 Ig, Placebo
3 · Its place in the literature

Who cites it

153 citing papers in PubMed, 4 syntheses or guidelines pooled it, 598 citations in OpenAlex.

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  15. The PKC inhibitor AEB071 may be a therapeutic option for psoriasis.The Journal of clinical investigation · 2008
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93 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

19 authors at 14 institutions in 4 countries.

J R AbramsBristol-Myers Squibb Pharmaceutical Research Institute, Wallingford, Connecticut 06492, USA.abramsj@bms.com
M G Lebwohl
C A Guzzo
B V Jegasothy
M T Goldfarb
B S Goffe
A Menter
N J Lowe
G Krueger
M J Brown
R S Weiner
M J Birkhofer
G L Warner
K K Berry
P S Linsley
J G Krueger
H D Ochs
S L Kelley
S Kang
Bristol-Myers Squibb (Germany) · DEBristol-Myers Squibb (United States) · USUniversity of Michigan–Ann Arbor · USBaylor University Medical Center · USClinical Research Associates · USIcahn School of Medicine at Mount Sinai · USPfizer (United States) · USRockefeller University · USRosetta Stone (United States) · USSt. James's Hospital · IEUniversity of Pennsylvania · USUniversity of Pittsburgh Medical Center · USUniversity of Utah · USUniversity of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Engagement of the B7 family of molecules on antigen-presenting cells with their T cell-associated ligands, CD28 and CD152 (cytotoxic T lymphocyte-associated antigen-4 [CTLA-4]), provides a pivotal costimulatory signal in T-cell activation. We investigated the role of the CD28/CD152 pathway in psoriasis in a 26-week, phase I, open-label dose-escalation study. The importance of this pathway in the generation of humoral immune responses to T cell-dependent neoantigens, bacteriophage phiX174 and keyhole limpet hemocyanin, was also evaluated. Forty-three patients with stable psoriasis vulgaris received 4 infusions of the soluble chimeric protein CTLA4Ig (BMS-188667). Forty-six percent of all study patients achieved a 50% or greater sustained improvement in clinical disease activity, with progressively greater effects observed in the highest-dosing cohorts. Improvement in these patients was associated with quantitative reduction in epidermal hyperplasia, which correlated with quantitative reduction in skin-infiltrating T cells. No markedly increased rate of intralesional T-cell apoptosis was identified, suggesting that the decreased number of lesional T cells was probably likely attributable to an inhibition of T-cell proliferation, T-cell recruitment, and/or apoptosis of antigen-specific T cells at extralesional sites. Altered antibody responses to T cell-dependent neoantigens were observed, but immunologic tolerance to these antigens was not demonstrated. This study illustrates the importance of the CD28/CD152 pathway in the pathogenesis of psoriasis and suggests a potential therapeutic use for this novel immunomodulatory approach in an array of T cell-mediated diseases.

Indexed as

ImmunoconjugatesLymphocyte ActivationAbataceptAdultAntibody FormationAntigens, CDAntigens, DifferentiationCohort StudiesCTLA-4 AntigenDose-Response Relationship, ImmunologicFemaleHumansImmunohistochemistryKeratinocytesMaleMiddle AgedAbataceptAntigens, CDAntigens, DifferentiationCTLA-4 AntigenCTLA4 protein, humanImmunoconjugates

Identifiers

PMID10225967
PMCPMC408469
OpenAlexW2137096190

What OpenQuestion holds

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Read underepoch 390

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.