Evidence map›Paper›PMID 40226621›Full record

ArticleFrontiers in immunology2025

BTLA agonist attenuates Th17-driven inflammation in a mouse model of steroid-resistant asthma.

Christine Quach, Xin Li, Pedram Shafiei-Jahani, Meng Li, Stephen Shen, Doumet Georges Helou, Benjamin P Hurrell, Pejman Soroosh, Omid Akbari

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

9 authors.

Christine QuachDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
Xin LiDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
Pedram Shafiei-JahaniDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
Meng LiUniversity of Southern California, Libraries Bioinformatics Service, University of Southern California, Los Angeles, CA, United States.
Stephen ShenDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
Doumet Georges HelouDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
Benjamin P HurrellDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
Pejman SorooshJanssen Research and Development, San Diego, CA, United States.
Omid AkbariDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.

Funding

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
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
$1.2M
NHLBI NIH HHS R01 HL144790NIAID NIH HHS R01 AI169687NIAID NIH HHS R01 AI181866
6 · The paper itself

Abstract

Introduction: Steroid-resistant asthma does not respond adequately to corticosteroid treatment. The underlying mechanisms driving corticosteroid resistance remain poorly understood, partly due to the absence of suitable animal models. Identifying the immunomodulatory pathways and mechanisms driving steroid resistance is crucial for developing effective therapies. Methods: In this study, we screened 58 murine strains exposed to house dust mite and identified that the BXD75 strain exhibited neutrophil-skewed, steroid-resistant asthma and elevated Th17 cells. RNA sequencing of lung CD4 Results: Transcriptomic analysis revealed increased HVEM expression and decreased BTLA expression, both critical immune regulators associated with stimulatory and inhibitory signaling, respectively. These T cells demonstrated enhanced inflammatory signaling through both canonical and non-canonical NF-κB pathways. BTLA agonist treatment Discussion: Our findings establish BXD75 mice as a model for steroid-resistant asthma and demonstrate that BTLA agonism attenuates airway hyperreactivity and lung inflammation, highlighting it as a potential therapeutic strategy.

Indexed as

AsthmaDrug ResistanceReceptors, ImmunologicTh17 CellsAnimalsDisease Models, AnimalFemaleInflammationLungMicePyroglyphidaeSignal TransductionBTLA protein, mouseReceptors, ImmunologicBTLAHVEMneutrophilic asthmasteroid-resistant asthmaTh17

Identifiers

PMID40226621
PMCPMC11986467

What Socratic 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 Socratic graph.