γ-Tocotrienol (GT3), a member of the vitamin E family, is well known for its medicinal value in clinical treatments. However, the role of GT3 in T helper 17 (Th17)/regulatory T cell (Treg) differentiation and function is not fully understood. Here, we demonstrated that GT3 suppressed Th17 differentiation in vitro by inhibiting signal transducer and activator of transcription 3 (STAT3) phosphorylation in the interleukin 6 (IL-6)/Janus kinase (JAK)/STAT3 signaling pathway. GT3 also inhibited HIF1A expression in Th17 metabolism. Additionally, we showed that GT3 treatment inhibited disease aggravation in an imiquimod (IMQ)-induced psoriasis-like mouse model by reducing the percentage of Th17 cells in the spleen in vivo. The findings of this study demonstrated the effects of GT3 on Th17 cells through the STAT3 signaling pathway.
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http://dx.doi.org/10.1016/j.molimm.2022.09.007 | DOI Listing |
Cell Rep
January 2025
Department of Genetics, St. Jude Children's Research Hospital, Memphis, TN 38105, USA; Department of Anatomy and Neurobiology, College of Graduate Health Sciences, University of Tennessee Health Science Center, Memphis, TN 38163, USA. Electronic address:
Neuraminidase 1 (NEU1) cleaves terminal sialic acids from sialoglycoproteins in endolysosomes and at the plasma membrane. As such, NEU1 regulates immune cells, primarily those of the monocytic lineage. Here, we examine how Neu1 influences microglia by modulating the sialylation of full-length Trem2 (Trem2-FL), a multifunctional receptor that regulates microglial survival, phagocytosis, and cytokine production.
View Article and Find Full Text PDFJ Virol
January 2025
Department of Veterinary Pathobiology, College of Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, Texas, USA.
The molecular mechanisms by which vaccinia virus (VACV), the prototypical member of the poxviridae family, reprograms host cell metabolism remain largely unexplored. Additionally, cells sense and respond to fluctuating nutrient availability, thereby modulating metabolic pathways to ensure cellular homeostasis. Understanding how VACV modulates metabolic pathways in response to nutrient signals is crucial for understanding viral replication mechanisms, with the potential for developing antiviral therapies.
View Article and Find Full Text PDFOMICS
January 2025
Department of Biotechnology, Brainware University, Barasat, West Bengal, India.
Next-generation cancer phenomics by deployment of multiple molecular endophenotypes coupled with high-throughput analyses of gene expression offer veritable opportunities for triangulation of discovery findings in non-small cell lung cancer (NSCLC) research. This study reports differentially expressed genes in NSCLC using publicly available datasets (GSE18842 and GSE229253), uncovering 130 common genes that may potentially represent crucial molecular signatures of NSCLC. Additionally, network analyses by GeneMANIA and STRING revealed significant coexpression and interaction patterns among these genes, with four notable hub genes-, , and -identified as pivotal in NSCLC progression.
View Article and Find Full Text PDFJ Asthma
January 2025
School of Pharmacy, Hubei University of Chinese Medicine, Wuhan, China.
Background: Studies have suggested associations between montelukast and increased risks of sleep disorders, including overall sleeping problems and insomnia. However, the results of observational studies are not consistent. Understanding these associations is crucial, particularly in patients solely diagnosed with allergic rhinitis, where montelukast use remains prevalent.
View Article and Find Full Text PDFIUBMB Life
January 2025
Department of General Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Tamoxifen (TAM) is employed to treat premenopausal ER-positive breast cancer patients, but TAM resistance is the main reason affecting its efficacy. Thus, addressing TAM resistance is crucial for improving therapeutic outcomes. This study explored the potential role of Tinagl1, a secreted extracellular matrix protein, whose expression is compromised in TAM-resistant MCF-7 breast cancer cells (MCF-7R).
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