Evidence map›Paper›PMID 34611329›Full record

ReviewNature reviews. Rheumatology2021

Targeting interferon-γ in hyperinflammation: opportunities and challenges.

Fabrizio De Benedetti, Giusi Prencipe, Claudia Bracaglia, Emiliano Marasco, Alexei A Grom

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
13.5field-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.

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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.

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  9. Adeno-Associated Virus Gene Therapy for Spinal Muscular Atrophy Induces Hepatotoxicity via Cytokine and Macrophage Activation.Liver international : official journal of the International Association for the Study of the Liver · 2026
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  11. Thrombaxane-B2 as a predictor marker of atrial fibrillation.International journal of cardiology. Cardiovascular risk and prevention · 2026
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20 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

5 authors at 2 institutions in 2 countries.

Fabrizio De BenedettiDivision of Rheumatology and Laboratory of ImmunoRheumatology, Ospedale Pediatrico Bambino Gesù, IRCCS, Roma, Italy. fabrizio.debenedetti@opbg.net.ORCID http://orcid.org/0000-0001-8749-8232
Giusi PrencipeDivision of Rheumatology and Laboratory of ImmunoRheumatology, Ospedale Pediatrico Bambino Gesù, IRCCS, Roma, Italy.
Claudia BracagliaDivision of Rheumatology and Laboratory of ImmunoRheumatology, Ospedale Pediatrico Bambino Gesù, IRCCS, Roma, Italy.
Emiliano MarascoDivision of Rheumatology and Laboratory of ImmunoRheumatology, Ospedale Pediatrico Bambino Gesù, IRCCS, Roma, Italy.
Alexei A GromDivision of Rheumatology, ML 4010, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.ORCID http://orcid.org/0000-0001-5717-136X
Bambino Gesù Children's Hospital · ITCincinnati Children's Hospital Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interferon-γ (IFNγ) is a pleiotropic cytokine with multiple effects on the inflammatory response and on innate and adaptive immunity. Overproduction of IFNγ underlies several, potentially fatal, hyperinflammatory or immune-mediated diseases. Several data from animal models and/or from translational research in patients point to a role of IFNγ in hyperinflammatory diseases, such as primary haemophagocytic lymphohistiocytosis, various forms of secondary haemophagocytic lymphohistiocytosis, including macrophage activation syndrome, and cytokine release syndrome, all of which are often managed by rheumatologists or in consultation with rheumatologists. Given the effects of IFNγ on B cells and T follicular helper cells, a role for IFNγ in systemic lupus erythematosus pathogenesis is emerging. To improve our understanding of the role of IFNγ in human disease, IFNγ-related biomarkers that are relevant for the management of hyperinflammatory diseases are progressively being identified and studied, especially because circulating levels of IFNγ do not always reflect its overproduction in tissue. These biomarkers include STAT1 (specifically the phosphorylated form), neopterin and the chemokine CXCL9. IFNγ-neutralizing agents have shown efficacy in the treatment of primary haemophagocytic lymphohistiocytosis in clinical trials and initial promising results have been obtained in various forms of secondary haemophagocytic lymphohistiocytosis, including macrophage activation syndrome. In clinical practice, there is a growing body of evidence supporting the usefulness of circulating CXCL9 levels as a biomarker reflecting IFNγ production.

Indexed as

AnimalsAntibodies, Monoclonal, HumanizedBiomarkersChemokine CXCL9Crohn DiseaseDisease Models, AnimalHumansImmune System DiseasesImmunityInflammationInterferon-gammaLymphohistiocytosis, HemophagocyticMacrophage Activation SyndromeMiceNeopterinSTAT1 Transcription FactorAntibodies, Monoclonal, HumanizedBiomarkersChemokine CXCL9CXCL9 protein, humanInterferon-gammaNeopterinSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID34611329
OpenAlexW3202912135

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.