ArticleCell death discovery2025
CXCL16 knockout inhibit asthma airway inflammation by suppressing H2-DM molecular mediated antigen presentation.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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.
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Who cites it
4 citing papers in PubMed.
- MAPK-driven glioma progression and reprogramming of the tumor-associated immune response.Neuro-oncology · 2026Article
- Effects and Mechanisms of Wrist-Ankle Acupuncture on Inflammatory Pain in the Rat Gastrocnemius Muscle.Journal of pain research · 2026Article
- Advancements in understanding and treating CXCL16/CXCR6 in tumors and in inflammatory diseases: a narrative review.Frontiers in immunology · 2026Review
- Impaired immune metabolism in COPD driven by dysfunction of CXCL16 + alveolar macrophages: multivariate causal evidence.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
The inflammatory microenvironment influences dendritic cell-mediated antigen presentation to regulate asthma Th2 inflammation. The scavenger receptor is expressed on DCs and regulates antigen presentation and T priming. However, whether the transmembrane scavenger receptor (SR-PSOX/CXCL16) regulates the phenotype and antigen presentation function of DCs remains unclear. We found that CXCL16 is mainly expressed on DCs in the lung tissues of asthma patients and asthma mice. CXCL16 knockout led to the suppression of airway inflammation, mucus overproduction, and airway hyperresponsiveness in Aspergillus-induced asthma. In addition, the adoptive transfer of Aspergillus-pulsed DCs shows the CXCL16
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Registered trials
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.