Evidence map›Paper›PMID 38172258›Full record

ArticleNature immunology2024

A type 1 immunity-restricted promoter of the IL-33 receptor gene directs antiviral T-cell responses.

Tobias M Brunner, Sebastian Serve, Anna-Friederike Marx, Jelizaveta Fadejeva, Philippe Saikali, Maria Dzamukova, Nayar Durán-Hernández, Christoph Kommer, Frederik Heinrich, Pawel Durek and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Nature immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 17 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

16 authors at 5 institutions in 2 countries.

Tobias M Brunner *Experimental Immunology and Osteoarthritis Research, Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. tobias.brunner@drfz.de.ORCID http://orcid.org/0000-0002-5279-2391
Sebastian Serve *Experimental Immunology and Osteoarthritis Research, Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0002-9839-7119
Anna-Friederike MarxDivision of Experimental Virology, Department of Biomedicine, University of Basel, Basel, Switzerland.
Jelizaveta FadejevaExperimental Immunology and Osteoarthritis Research, Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Philippe SaikaliExperimental Immunology and Osteoarthritis Research, Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0002-4916-7376
Maria DzamukovaExperimental Immunology and Osteoarthritis Research, Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0002-2389-3222
Nayar Durán-HernándezExperimental Immunology and Osteoarthritis Research, Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0003-4253-0387
Christoph KommerDivision of Theoretical Systems Biology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Frederik HeinrichTherapeutic Gene Regulation, German Rheumatism Research Center (DRFZ), a Leibniz Institute, Berlin, Germany.ORCID http://orcid.org/0000-0001-6097-5422
Pawel DurekTherapeutic Gene Regulation, German Rheumatism Research Center (DRFZ), a Leibniz Institute, Berlin, Germany.
Gitta A HeinzTherapeutic Gene Regulation, German Rheumatism Research Center (DRFZ), a Leibniz Institute, Berlin, Germany.ORCID http://orcid.org/0000-0002-9330-3689
Thomas HöferDivision of Theoretical Systems Biology, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID http://orcid.org/0000-0003-3560-8780
Mir-Farzin MashreghiTherapeutic Gene Regulation, German Rheumatism Research Center (DRFZ), a Leibniz Institute, Berlin, Germany.ORCID http://orcid.org/0000-0002-8015-6907
Ralf KühnMax Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany.ORCID http://orcid.org/0000-0003-1694-9803
Daniel D PinschewerDivision of Experimental Virology, Department of Biomedicine, University of Basel, Basel, Switzerland.ORCID http://orcid.org/0000-0002-1594-3189
Max LöhningExperimental Immunology and Osteoarthritis Research, Department of Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. max.loehning@charite.de.ORCID http://orcid.org/0000-0001-6382-7281
Humboldt-Universität zu Berlin · DEGerman Rheumatism Research Centre · DEGerman Cancer Research Center · DEUniversity of Basel · CHMax Delbrück Center · DE

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) LO 1542/4-1Deutsche Forschungsgemeinschaft (German Research Foundation) LO 1542/5-1EC | European Regional Development Fund (Europski Fond za Regionalni Razvoj) EFRE 1.8/11EC | European Regional Development Fund (Europski Fond za Regionalni Razvoj) ERDF 2014-2020Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation) 310030_185318/1Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation) CRSII3_160772/1
6 · The paper itself

Abstract

The pleiotropic alarmin interleukin-33 (IL-33) drives type 1, type 2 and regulatory T-cell responses via its receptor ST2. Subset-specific differences in ST2 expression intensity and dynamics suggest that transcriptional regulation is key in orchestrating the context-dependent activity of IL-33-ST2 signaling in T-cell immunity. Here, we identify a previously unrecognized alternative promoter in mice and humans that is located far upstream of the curated ST2-coding gene and drives ST2 expression in type 1 immunity. Mice lacking this promoter exhibit a selective loss of ST2 expression in type 1- but not type 2-biased T cells, resulting in impaired expansion of cytotoxic T cells (CTLs) and T-helper 1 cells upon viral infection. T-cell-intrinsic IL-33 signaling via type 1 promoter-driven ST2 is critical to generate a clonally diverse population of antiviral short-lived effector CTLs. Thus, lineage-specific alternative promoter usage directs alarmin responsiveness in T-cell subsets and offers opportunities for immune cell-specific targeting of the IL-33-ST2 axis in infections and inflammatory diseases.

Indexed as

Interleukin-1 Receptor-Like 1 ProteinInterleukin-33AlarminsAnimalsAntiviral AgentsHumansMiceT-Lymphocyte SubsetsAlarminsAntiviral AgentsIL1RL1 protein, humanIl1rl1 protein, mouseInterleukin-1 Receptor-Like 1 ProteinInterleukin-33

Identifiers

PMID38172258
PMCPMC10834369
OpenAlexW4390572229

What OpenQuestion holds

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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.