Targeting their activation states and signaling pathways represents a promising avenue for mechanism-guided AF therapy. Therefore, this review provides a consolidated framework for future translational strategies aiming to interrupt the immune-mediated remodeling cascade in AF.
We proposed a non-invasive prediction method based on TEX-related genes, which effectively predicts survival outcomes and therapeutic responses in COAD patients. Additionally, FAT4 was found to regulate proliferative and apoptotic phenotypes in COAD.
This study provides insights into the mechanisms by which plasma lipid metabolism influences kidney stone development through inflammatory regulatory networks. These findings lay a theoretical foundation for lipidomics- and inflammation-based biomarker risk prediction, as well as targeted intervention strategies for kidney stone prevention.
Our findings establish a novel radiogenomic strategy that bridges MRI-derived imaging phenotypes with molecular mechanisms. FIBCD1 may serve as an immune-modulating prognostic biomarker linked to imaging characteristics, providing new insights into non-invasive breast cancer risk assessment and therapeutic targeting.
These LIGHT-mediated structural alterations synergize with damage-associated molecular patterns (DAMPs) released from pyroptotic cells, collectively promoting the infiltration, and activation of immune cells into the tumor site, further potentiating the anti-tumor immune response. This study establishes a novel therapeutic paradigm against GBM immunosuppressive TME through the synergistic effect of immunogenic cell death, metabolic reprogramming, and immune amplification.
The expression levels of immune checkpoint genes CD276, CD40, and TNFSF14 related to copper death are positively correlated with the prognosis of GBM patients, while the expression level of TNFSF9 is negatively correlated with the prognosis of GBM patients. This study establishes a novel link between immune checkpoint genes and cuproptosis, bridging copper-induced cell death mechanisms with immunotherapy for glioma.
We identified altered protein expression and an increased IFN system activation in SjD with incident lymphoma and pre-lymphoma. This knowledge may contribute to earlier detection of high-risk patients, identification of therapeutic targets and may ultimately improve SjD patient outcomes.
Inhibiting LSD1 in GC upregulates TNFSF14 expression, which in turn promotes T cell proliferation, CD8+ activation, and chemotaxis. This enhancement of T cell-mediated anti-tumor immunity is further amplified when LSD1 inhibitors are used alongside PD-(L)1 blockers, facilitating the activation of CD8+ T cells in the spleen and improving leukocyte infiltration in the tumor.
Expression of LIGHT in atherosclerotic plaques not only correlates with markers of plaque destabilization, but is also significantly elevated in plaques from symptomatic compared to those from asymptomatic patients. These results associate LIGHT content with a rupture-prone plaque phenotype, potentially upregulated as part of a reparative response, warranting further studies.
Whereas both LIGHT overexpression and anti-CTLA-4 increase tumor-promoting macrophages, the combination eliminates this population. The ability of LIGHT overexpression combined with CTLA-4 inhibition to reverse T cell exhaustion and myeloid cell suppression is supported by analysis of complementary patient cohorts and has strong clinical relevance, especially given that liver metastases contribute to immunotherapy resistance across various cancer types.
We explore the molecular mechanisms of LIGHT signalling through its receptors, Herpes Virus Entry Mediator (HVEM) and Lymphotoxin-β Receptor (LTβR), and how these distinct interactions dictate its pro-inflammatory or regulatory functions. Finally, we review the therapeutic potential of targeting this pathway, highlighting the results of recent clinical trials and exploring future strategies aimed at restoring immune homeostasis in patients with IBD.