ArticleScientific reports2025
Immune genes CD247 STAT1 and LCK mediate host-pathogen interactions in sporotrichosis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Sporotrichosis is a chronic subcutaneous infection caused by the Sporothrix complex, a dimorphic fungus that exhibits significant clinical heterogeneity. However, the molecular targets and underlying mechanisms of Sporothrix globosa infection remain unclear. Therefore, in this study, we aimed to integrate whole-transcriptome sequencing analysis of skin lesion tissues from patients with sporotrichosis and healthy controls. In addition, differential gene expression screening, protein-protein interaction network construction, and functional enrichment analysis. We systematically identified the key immune-related genes, Cluster of Differentiation 247 (CD247), Signal Transducer and Activator of Transcription 1 (STAT1), and Lymphocyte-Specific Tyrosine Kinase (LCK), which are majorly upregulated during infections. The high expression of these genes in the disease group was consistently validated by western blot, quantitative polymerase chain reaction, and immunohistochemistry. Mechanistic analysis revealed the contribution of these genes to sporotrichosis-dysregulated immune response. This occurs by causing excessive activation of the interferon signaling pathway, lymphocyte overactivation, and the JAK-STAT signaling pathway, which leads to the host immune imbalance. This suggests their central role in immune evasion and overactivation during sporotrichosis. In this novel study, we revealed the pathological regulatory role of the CD247-STAT1-LCK molecular network in sporotrichosis, which provided novel insights into fungal-host interactions and identified potential therapeutic targets for immune-modulating antifungal treatments.
Indexed as
Identifiers
What OpenQuestion holds
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.