Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing 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.
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
10 authors.
Yoshihiro SakanoDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.ORCID 0000-0002-7633-6657
Kei SakanoDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.ORCID 0000-0002-0504-1691
Kota KokuboDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.ORCID 0000-0001-6896-1981
Benjamin P HurrellDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Stephen ShenDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.ORCID 0000-0002-8417-1880
Xin LiDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.ORCID 0000-0002-2050-2628
Gowri Yeliyur Shivakumara SwamyDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Jafar CainDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.ORCID 0009-0002-8959-4978
Vijay K KuchrooGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA, USA.
Omid AkbariDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA. akbari@usc.edu.ORCID 0000-0002-4359-9725
Funding
Study the link of autophagy dysfunction to allergic and neutrophilic asthma onsetR01HL151493 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI AKBARI, OMID · 2020 to 2024
$3.6M
Maternal effect on offspring immunity against hepatitis B virusR01AI145813 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI AKBARI, OMID, OU, J.-H. JAMES · 2019 to 2023
$3.2M
Role of TNF receptor 2 on Pulmonary Group 2 Innate Lymphoid CellsR01HL159804 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI AKBARI, OMID · 2022 to 2025
$3.0M
Induction of cells and pathways that promote respiratory tolerance in allergic asthmaR01HL144790 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI AKBARI, OMID · 2019 to 2022
$2.6M
E-Cigarette Vaping during Pregnancy and Lactation, Germ Cell Epigenetic Memory, and Transgenerational AsthmaR01HL151769 · NHLBI · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI ALLARD, PATRICK, REHAN, VIRENDER K · 2020 to 2023
$2.3M
Transcriptional and metabolomic regulation of IL-10 in pulmonary ILC2sR01AI169687 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI OMID AKBARI · 2022 to 2026
$2.1M
Study the role of ICOS on murine and human ILC2sR01AI181866 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI OMID AKBARI · 2025 to 2026
Allergic asthma is promoted by type 2 inflammation involving cytokines such as IL-4, IL-5, and IL-13, with group 2 innate lymphoid cells (ILC2s) playing a key pathogenic role. Here, we identify T cell immunoglobulin and mucin domain-containing protein 3 (Tim-3) as a negative regulator of ILC2 function. Tim-3 expression is upregulated in activated pulmonary ILC2s, and engagement with Tim-3 agonists inhibits ILC2 activation, proliferation, and type 2 cytokine production via the Nemo Like Kinase (NLK) signaling pathway and suppression of mitochondrial metabolism. In vivo, Tim-3 agonists alleviate airway hyperreactivity (AHR) and inflammation in both IL-33- and Alternaria alternata-induced AHR models, while ILC2-specific Tim-3 deletion exacerbates AHR. These results are confirmed in human ILC2s and humanized mice, supporting the translational relevance. Our findings establish Tim-3 as an inhibitory checkpoint for ILC2s and suggest its potential as a therapeutic target in allergic asthma and other ILC2-mediated diseases.
Indexed as
AsthmaHepatitis A Virus Cellular Receptor 2Immunity, InnateLymphocytesAlternariaAnimalsCytokinesFemaleHumansInterleukin-33LungMiceMice, Inbred C57BLMice, KnockoutSignal TransductionCytokinesHAVCR2 protein, humanHavcr2 protein, mouseHepatitis A Virus Cellular Receptor 2Interleukin-33
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.
Tim-3 agonist restrains ILC2 function and attenuates airway hyperreactivity via NLK pathway. · full record | OpenQuestion