Results 121 to 130 of about 174,472 (265)
O‐GlcNAcylated TAP1 Impairs Antigen Presentation and Promotes Immune Evasion in Bladder Cancer
This article unveils a critical mechanism of immune evasion in bladder cancer, which the O‐GlcNAc modification of TAP1 disrupts antigen presentation. This modification triggers HLA‐A degradation, shielding tumor cells from CD8+ T cell attack. The findings highlight targeting this pathway as a promising therapeutic avenue to sensitize tumors to ...
Jinpeng Wu +10 more
wiley +1 more source
ABSTRACT Liver metastasis is a leading cause of mortality in colorectal cancer (CRC), where the inflammatory tumor microenvironment, specifically neutrophil infiltration, significantly promotes metastatic colonization. This study reveals a pro‐metastatic role for alpha‐1 antitrypsin (A1AT) in CRC liver metastasis via a dual mechanism involving ...
Qian Fei +11 more
wiley +1 more source
A single‐cell atlas of pancreatic ductal adenocarcinoma development reveals progressive ductal‐fibroblast‐immune crosstalk. Tumor‐derived LAMB3 drives the formation of immunosuppressive LRRC15+ fibroblasts through the ITGB1/FAK/MAPK/FOSL2 signaling. Glycolytic reprogramming upregulates LAMB3 and correlates with LRRC15+ fibroblast enrichment.
Xuqing Shi +23 more
wiley +1 more source
A Microbial Lipid‐ATP Synthase Axis Fuels NK Cell Antitumor Activity
This study focuses on the mechanism by which gut microbiota‐derived outer membrane vesicles (OMVs) regulate NK cell antitumor activity. B. intestinalis is identified to decrease extra‐intestinal tumor growth via its OMVs enriched in sphingosine (SP).
Kaiyuan Yu +16 more
wiley +1 more source
Macrophage Extracellular Traps in Immunity and Cancer
As a macrophage‐mediated innate defense mechanism, the dysregulated release of METs drives chronic inflammation and influences tumor progression. Furthermore, METs exhibit a functional duality within the tumor microenvironment, capable of both promoting and suppressing tumor development.
Junyao Li +5 more
wiley +1 more source
m6A‐Mediated Glycolysis by IL‐37 Drives T Cell Metabolic Reprogramming to Regulate Colitis
This study identifies an IL‐37/SIGIRR‐METTL14 regulatory axis that suppresses global m6A modification in CD4+ T cells. IL‐37 signaling, mediated through SIGIRR, inhibits IRAK4 and JNK phosphorylation, leading to downregulation of the methyltransferase METTL14.
Xiaoyan Wang +26 more
wiley +1 more source
In rheumatoid arthritis, synovial Tregs accumulate but are functionally impaired due to iron overload‐induced ferroptosis. This triggers mitochondrial dysfunction and TXK tyrosine kinase‐mediated signaling, leading to Treg destabilization and inflammation.
Jingrong Chen +19 more
wiley +1 more source
T Cell Exhaustion in Cancer Immunotherapy: Heterogeneity, Mechanisms, and Therapeutic Opportunities
T cell exhaustion limits immunotherapy efficacy. This article delineates its progression from stem‐like to terminally exhausted states, governed by persistent antigen, transcription factors, epigenetics, and metabolism. It maps the exhaustion landscape in the TME and proposes integrated reversal strategies, providing a translational roadmap to overcome
Yang Yu +7 more
wiley +1 more source
Lymphoid‐Tissue‐on‐Chip Recapitulates Human Antibody Responses In Vitro
The presented lymphoid‐tissue‐on‐chip system allows culture of primary human tonsil cells at organotypic high density under perfusion for up to 4 weeks, emulates immune response to soluble vaccines and vaccination via peripheral antigen‐presenting cells and represents a useful tool to assess cellular interactions during homeostasis, immune responses ...
Claudia Teufel +15 more
wiley +1 more source
HNRNPD promotes radioresistance in nasopharyngeal carcinoma by enhancing stress granule assembly and sequestering GRAMD4 mRNA. This suppresses GRAMD4 translation and inhibits mitochondrial apoptosis. Targeting the integrated stress response with ISRIB restores GRAMD4 expression and sensitizes tumors to radiotherapy, revealing a translational control ...
Yingzi Li +13 more
wiley +1 more source

