Evidence map›Paper›PMID 35746582›Full record

ReviewVaccines2022

Biological Therapy of Severe Asthma with Dupilumab, a Dual Receptor Antagonist of Interleukins 4 and 13.

Corrado Pelaia, Giulia Pelaia, Claudia Crimi, Angelantonio Maglio, Giuseppe Armentaro, Cecilia Calabrese, Angela Sciacqua, Luca Gallelli, Alessandro Vatrella

Open access · goldAbstract readReview
In one paragraph

Review in Vaccines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 25 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 4 institutions in 1 country.

Corrado PelaiaDepartment of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.ORCID 0000-0002-4236-7367
Giulia PelaiaDepartment of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Claudia CrimiDepartment of Clinical and Experimental Medicine, University of Catania, 95123 Catania, Italy.ORCID 0000-0002-9088-5214
Angelantonio MaglioDepartment of Medicine, Surgery and Dentistry, University of Salerno, 84084 Salerno, Italy.ORCID 0000-0003-1874-1686
Giuseppe ArmentaroDepartment of Medical and Surgical Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.ORCID 0000-0001-9775-9715
Cecilia CalabreseDepartment of Translational Medical Sciences, University of Campania "Luigi Vanvitelli", 80131 Naples, Italy.ORCID 0000-0003-4293-4461
Angela SciacquaDepartment of Medical and Surgical Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Luca GallelliDepartment of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.ORCID 0000-0003-0858-7902
Alessandro VatrellaDepartment of Medicine, Surgery and Dentistry, University of Salerno, 84084 Salerno, Italy.ORCID 0000-0001-8265-3037
Magna Graecia University · ITUniversity of Salerno · ITUniversity of Campania "Luigi Vanvitelli" · ITUniversity of Catania · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin-4 (IL-4) and interleukin-13 (IL-13) are key cytokines involved in the pathophysiology of both immune-inflammatory and structural changes underlying type 2 asthma. IL-4 plays a pivotal role in Th2 cell polarization, immunoglobulin E (IgE) synthesis and eosinophil recruitment into the airways. IL-13 synergizes with IL-4 in inducing IgE production and also promotes nitric oxide (NO) synthesis, eosinophil chemotaxis, bronchial hyperresponsiveness and mucus secretion, as well as the proliferation of airway resident cells such as fibroblasts and smooth muscle cells. The biological effects of IL-4 and IL-13 are mediated by complex signaling mechanisms activated by receptor dimerization triggered by cytokine binding to the α-subunit of the IL-4 receptor (IL-4Rα). The fully human IgG4 monoclonal antibody dupilumab binds to IL-4Rα, thereby preventing its interactions with both IL-4 and IL-13. This mechanism of action makes it possible for dupilumab to effectively inhibit type 2 inflammation, thus significantly reducing the exacerbation of severe asthma, the consumption of oral corticosteroids (OCS) and the levels of fractional exhaled NO (FeNO). Dupilumab has been approved not only for the add-on therapy of severe asthma, but also for the biological treatment of atopic dermatitis and nasal polyposis.

Indexed as

dupilumabIL-13IL-4severe asthma

Identifiers

PMID35746582
PMCPMC9229960
OpenAlexW4283172083

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.