Evidence map›Paper›PMID 40089475›Full record

ArticleNature communications2025

Single-cell and chromatin accessibility profiling reveals regulatory programs of pathogenic Th2 cells in allergic asthma.

Matarr Khan, Marlis Alteneder, Wolfgang Reiter, Thomas Krausgruber, Lina Dobnikar, Moritz Madern, Monika Waldherr, Christoph Bock, Markus Hartl, Wilfried Ellmeier and 2 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
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

12 authors.

Matarr KhanMedical University of Vienna, Center of Pathophysiology, Infectiology and Immunology, Institute of Immunology, Division of Immunobiology, Vienna, Austria.
Marlis AltenederMedical University of Vienna, Center of Pathophysiology, Infectiology and Immunology, Institute of Immunology, Division of Immunobiology, Vienna, Austria.
Wolfgang ReiterMax Perutz Labs, Mass Spectrometry Facility, Vienna Biocenter Campus (VBC), Vienna, Austria.ORCID http://orcid.org/0000-0003-1266-8975
Thomas KrausgruberCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID http://orcid.org/0000-0002-1374-0329
Lina DobnikarCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Moritz MadernMedical University of Vienna, Center of Pathophysiology, Infectiology and Immunology, Institute of Immunology, Division of Immunobiology, Vienna, Austria.ORCID http://orcid.org/0000-0001-8593-5785
Monika WaldherrMedical University of Vienna, Center of Pathophysiology, Infectiology and Immunology, Institute of Immunology, Division of Immunobiology, Vienna, Austria.ORCID http://orcid.org/0000-0003-1284-0616
Christoph BockCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID http://orcid.org/0000-0001-6091-3088
Markus HartlMax Perutz Labs, Mass Spectrometry Facility, Vienna Biocenter Campus (VBC), Vienna, Austria.ORCID http://orcid.org/0000-0002-4970-7336
Wilfried EllmeierMedical University of Vienna, Center of Pathophysiology, Infectiology and Immunology, Institute of Immunology, Division of Immunobiology, Vienna, Austria.ORCID http://orcid.org/0000-0001-8192-8481
Johan HenrikssonUmeå University, Umeå Centre for Microbial Research (UCMR), Integrated Science Lab (Icelab), Department of Molecular Biology, Umeå, Sweden.ORCID http://orcid.org/0000-0002-7745-2844
Nicole BoucheronMedical University of Vienna, Center of Pathophysiology, Infectiology and Immunology, Institute of Immunology, Division of Immunobiology, Vienna, Austria. nicole.boucheron@meduniwien.ac.at.ORCID http://orcid.org/0000-0002-4979-8311

Funding

Austrian Science Fund (Fonds zur Förderung der Wissenschaftlichen Forschung) F7004Austrian Science Fund (Fonds zur Förderung der Wissenschaftlichen Forschung) P30885Cancerfonden (Swedish Cancer Society) #23 3102 PjVetenskapsrådet (Swedish Research Council) #2021-06602Vetenskapsrådet (Swedish Research Council) #2024-03952
6 · The paper itself

Abstract

Lung pathogenic T helper type 2 (pTh2) cells are important in mediating allergic asthma, but fundamental questions remain regarding their heterogeneity and epigenetic regulation. Here we investigate immune regulation in allergic asthma by single-cell RNA sequencing in mice challenged with house dust mite, in the presence and absence of histone deacetylase 1 (HDAC1) function. Our analyses indicate two distinct highly proinflammatory subsets of lung pTh2 cells and pinpoint thymic stromal lymphopoietin (TSLP) and Tumour Necrosis Factor Receptor Superfamily (TNFRSF) members as important drivers to generate pTh2 cells in vitro. Using our in vitro model, we uncover how signalling via TSLP and a TNFRSF member shapes chromatin accessibility at the type 2 cytokine gene loci by modulating HDAC1 repressive function. In summary, we have generated insights into pTh2 cell biology and establish an in vitro model for investigating pTh2 cells that proves useful for discovering molecular mechanisms involved in pTh2-mediated allergic asthma.

Indexed as

AsthmaChromatinTh2 CellsAnimalsCytokinesEpigenesis, GeneticFemaleLungMiceMice, Inbred C57BLPyroglyphidaeSingle-Cell AnalysisThymic Stromal LymphopoietinChromatinCytokinesThymic Stromal Lymphopoietin

Identifiers

PMID40089475
PMCPMC11910648

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.