Evidence map›Paper›PMID 41015960›Full record

ReviewInflammopharmacology2025

Interleukin-10 family cytokines: key regulators and novel therapeutic targets for respiratory diseases.

Pouya Goleij, Alireza Amini, Sajad Abolfazli, Mohammad Mahdi Heidari, Mohammad Amin Khazeei Tabari, Michael Aschner, Danaé S Larsen, Haroon Khan, Maria Daglia

Abstract readReview
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In one paragraph

Review in Inflammopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Pouya GoleijUSERN Office, Kermanshah University of Medical Sciences, Kermanshah, 6715847141, Iran. medgenetic.1991@gmail.com.ORCID http://orcid.org/0000-0002-2213-497X
Alireza AminiStudent Research Committee, School of Medicine, Mazandaran University of Medical Sciences, Mazandaran, 4815733971, Iran.
Sajad AbolfazliStudent Research Committee, School of Pharmacy, Mazandaran University of Medical Sciences, Mazandaran, 4815733971, Iran.
Mohammad Mahdi HeidariDepartment of Pediatrics, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Mohammad Amin Khazeei TabariStudent Research Committee, School of Medicine, Mazandaran University of Medical Sciences, Mazandaran, 4815733971, Iran.
Michael AschnerDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, Forchheimer 209, 1300 Morris Park Avenue, Bronx, NY, 10461, USA.
Danaé S LarsenSchool of Chemical Sciences, The University of Auckland, 23 Symonds Street, Auckland, 1010, New Zealand.
Haroon KhanDepartment of Pharmacy, Faculty of Chemical and Life Sciences, Abdul Wali Khan University Mardan, Mardan, 23200, Pakistan. haroonkhan@awkum.edu.pk.
Maria DagliaDepartment of Pharmacy, University of Naples "Federico II", Via D. Montesano 49, 80131, Naples, Italy. maria.daglia@unina.it.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Respiratory disorders such as asthma, chronic obstructive pulmonary disease (COPD), acute respiratory distress syndrome (ARDS), pulmonary fibrosis, and infectious conditions including COVID-19 and tuberculosis continue to rank among the foremost causes of illness and death worldwide. Although vaccines, antimicrobial treatments, and anti-inflammatory agents have improved disease management, their overall impact remains limited because of the intricate regulation of immune responses at epithelial surfaces. Within this context, the interleukin-10 (IL-10) cytokine family (comprising IL-10, IL-19, IL-20, IL-22, IL-24, and IL-26) has been identified as a key immunological axis in the respiratory tract. These cytokines possess structural homology and predominantly transmit signals through heterodimeric class II receptors via the JAK-STAT cascade. However, their functions are far from uniform: IL-10 primarily exerts suppressive effects on inflammation, whereas IL-19, IL-20, IL-24, and IL-26 are commonly associated with tissue injury, chronic inflammation, and airway remodeling. IL-22 occupies an intermediate role, promoting epithelial regeneration under certain conditions but aggravating inflammation or tumorigenesis in others. This article reviews recent findings on the IL-10 family in a range of respiratory diseases, emphasizing their context-dependent activity, value as potential biomarkers, and relevance as therapeutic targets. A clearer understanding of how protective versus pathogenic signals are balanced within this cytokine network is essential for designing targeted interventions that preserve host defense while restoring airway integrity.

Indexed as

Interleukin-10Respiratory Tract DiseasesAnimalsCOVID-19HumansInflammationIL10 protein, humanInterleukin-10ARDS/COVID-19AsthmaCOPDCystic fibrosisEpithelial barrierIL-10 familyIL-19IL-20IL-22IL-24IL-26JAK–STATPulmonary fibrosisPulmonary infectionsRespiratory diseasesTherapeutic targets

Identifiers

PMID41015960

What Socratic 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 Socratic graph.