Evidence map›Paper›PMID 33463541›Full record

ReviewThe Journal of clinical investigation2021

IL-36 in chronic inflammation and fibrosis - bridging the gap?

Michael Elias, Shuai Zhao, Hongnga T Le, Jie Wang, Markus F Neurath, Clemens Neufert, Claudio Fiocchi, Florian Rieder

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 2 pooled it
6.7field-weighted citation impact, top 2% 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

74 citing papers in PubMed, 2 syntheses or guidelines pooled it, 108 citations in OpenAlex.

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  15. The Immune Microenvironment: New Therapeutic Implications in Organ Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
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14 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

8 authors at 2 institutions in 3 countries.

Michael EliasDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Shuai ZhaoDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Hongnga T LeDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Jie WangDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Markus F NeurathDepartment of Medicine 1 and Deutsches Zentrum Immuntherapie DZI, Universitaetsklinikum Erlangen, University of Erlangen-Nürnberg, Erlangen, Germany.
Clemens NeufertDepartment of Medicine 1 and Deutsches Zentrum Immuntherapie DZI, Universitaetsklinikum Erlangen, University of Erlangen-Nürnberg, Erlangen, Germany.
Claudio FiocchiDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Florian RiederDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Cleveland Clinic · USUniversitätsklinikum Erlangen · DE

Funding

The Cleveland Digestive Diseases Research Core Center (DDRCC)P30DK097948 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI AMITABH CHAK · 2015 to 2026
$15.6M
Creeping fat and Crohn's disease associated stricturesR01DK123233 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI RIEDER, FLORIAN · 2020 to 2024
$1.9M
NIDDK NIH HHS P30 DK097948NIDDK NIH HHS R01 DK123233
6 · The paper itself

Abstract

IL-36 is a member of the IL-1 superfamily and consists of three agonists and one receptor antagonist (IL-36Ra). The three endogenous agonists, IL-36α, -β, and -γ, act primarily as proinflammatory cytokines, and their signaling through the IL-36 receptor (IL-36R) promotes immune cell infiltration and secretion of inflammatory and chemotactic molecules. However, IL-36 signaling also fosters secretion of profibrotic soluble mediators, suggesting a role in fibrotic disorders. IL-36 isoforms and IL-36 have been implicated in inflammatory diseases including psoriasis, arthritis, inflammatory bowel diseases, and allergic rhinitis. Moreover, IL-36 has been connected to fibrotic disorders affecting the kidney, lung, and intestines. This review summarizes the expression, cellular source, and function of IL-36 in inflammation and fibrosis in various organs, and proposes that IL-36 modulation may prove valuable in preventing or treating inflammatory and fibrotic diseases and may reveal a mechanistic link between inflammation and fibrosis.

Indexed as

Gene Expression RegulationAnimalsFibrosisHumansInterleukin-1Organ SpecificityIL36A protein, humanIL36B protein, humanIL36G protein, humanInterleukin-1

Identifiers

PMID33463541
PMCPMC7810483
OpenAlexW3126064265

What OpenQuestion 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 OpenQuestion graph.