Evidence map›Paper›PMID 29943154›Full record

ArticleMolecular diagnosis & therapy2018

The Presence of HLA-A Bw4-80I KIR Ligands Could Predict "Difficult-to-Treat" Psoriasis and Poor Response to Etanercept.

M Guarene, A Pasi, V Bolcato, R Cananzi, A Piccolo, I Sbarsi, C Klersy, R Cacciatore, Valeria Brazzelli

Abstract read
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In one paragraph

Article in Molecular diagnosis & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

M GuareneImmunogenetics Laboratory, Immunohematology and Transfusion Centre, IRCCS Policlinico San Matteo Foundation, University of Pavia, Pavia, Italy.
A PasiImmunogenetics Laboratory, Immunohematology and Transfusion Centre, IRCCS Policlinico San Matteo Foundation, University of Pavia, Pavia, Italy.
V BolcatoInstitute of Dermatology, IRCCS Policlinico San Matteo Foundation, University of Pavia, Piazzale Golgi, 2, 27100, Pavia, Italy.
R CananziInstitute of Dermatology, IRCCS Policlinico San Matteo Foundation, University of Pavia, Piazzale Golgi, 2, 27100, Pavia, Italy.
A PiccoloUnit of Anatomic Pathology, Department of Molecular Medicine, IRCCS Policlinico San Matteo Foundation, University of Pavia, Pavia, Italy.
I SbarsiImmunogenetics Laboratory, Immunohematology and Transfusion Centre, IRCCS Policlinico San Matteo Foundation, University of Pavia, Pavia, Italy.
C KlersyClinical Epidemiology and Biometric Unit, IRCCS Policlinico San Matteo Foundation, University of Pavia, Pavia, Italy.
R CacciatoreImmunogenetics Laboratory, Immunohematology and Transfusion Centre, IRCCS Policlinico San Matteo Foundation, University of Pavia, Pavia, Italy.
Valeria BrazzelliInstitute of Dermatology, IRCCS Policlinico San Matteo Foundation, University of Pavia, Piazzale Golgi, 2, 27100, Pavia, Italy. vbrazzelli@libero.it.ORCID http://orcid.org/0000-0001-5898-6448
University of Pavia · IT

Funding

Ricerca corrente , IRCCS Policlinico San Matteo Foundation, University of Pavia, Pavia, Italy. 17794/2014
6 · The paper itself

Abstract

backgroundPsoriasis is an immune-mediated dermatosis with a wide genetic predisposition. The immunogenetic background, specifically interactions between human leukocyte antigen (HLA) class I ligands and killer-cell immunoglobulin-like receptor (KIRs), have functional significance in modulating natural killer (NK) cells and can influence susceptibility and response to biological therapy.

objectiveThe main aim of this study was to correlate HLA-A and -B KIR ligands with response to biological therapy in patients with psoriasis.

methodsHLA-A and -B polymorphisms were determined in 48 patients (35 males and 13 females), with a mean of 22 years of disease (range 8-55). All patients were treated with biological therapy (adalimumab, etanercept, infliximab, or ustekinumab) for at least 6 months.

resultsThis study identifies, with statistical significance, the presence of at least one ligand HLA-A Bw4-80I in the "poor-responder" population (patients who needed two or more biologics) compared with the "responder" population (patients with good response after a single biological drug) (47.62 vs. 11.11%; p = 0.006) as well as in "non-responders to etanercept" compared with "responders to etanercept" (52.63 vs. 5%; p = 0.001).

conclusionOur preliminary results suggest that at least one ligand HLA-A Bw4-80I could be associated with "difficult-to-treat" psoriasis and that this ligand may reduce the probability of response to etanercept, producing more tumor necrosis factor (TNF)-α and neutralizing NK activity through a predominance of activating KIR. The ab initio identification of genetic markers of response to biologic therapy could improve the efficacy and economic impact of these agents.

Indexed as

Polymorphism, GeneticAdalimumabAdolescentAdultBiological ProductsChildEtanerceptFemaleHLA-A AntigensHLA-B AntigensHumansInfliximabMaleMiddle AgedPsoriasisReceptors, KIRAdalimumabBiological ProductsEtanerceptHLA-A AntigensHLA-B AntigensHLA-Bw4 antigenInfliximabReceptors, KIRUstekinumab

Identifiers

PMID29943154
OpenAlexW2809887786

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Registered trials

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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.