Results 211 to 220 of about 275,584 (397)
The development of a novel engineered strain of Lactiplantibacillus plantarum (Lp) is reported that can produce bacterial extracellular vesicles (BEVs) at >60‐fold higher yields than the unmodified parental strain. These Lp BEVs retain therapeutic bioactivity as validated in a mouse model of dextran sodium sulfate‐induced colitis.
Nicholas H Pirolli +16 more
wiley +1 more source
In hepatocellular carcinoma (HCC), aberrantly activated Notch1 signaling induces its target gene YY1, which impairs immunotherapy efficacy by suppressing tumor cell‐ICAM1‐driven T cell activation and the mediated pyroptosis of T cells against tumor cells.
Ke Zhu +10 more
wiley +1 more source
Single‐cell sequencing reveals stress‐programmed immune states driving TNFα–TNFR2–mediated Treg activation and therapy resistance in breast cancer, while targeting this axis restores antitumor immunity. ABSTRACT The tumor microenvironment (TME) harbors diverse immune cell states that shape therapeutic outcomes in breast cancer.
Zhibo Shao +18 more
wiley +1 more source
A novel FOXP3 knockout-humanized mouse model for pre-clinical safety and efficacy evaluation of Treg-like cell products [PDF]
Yohei Sato +7 more
openalex +1 more source
Treg-Cell-Derived IL-35-Coated Extracellular Vesicles Promote Infectious Tolerance
Jeremy A. Sullivan +16 more
openalex +1 more source
Aberrant Muscle Antigen Exposure in Mice Is Sufficient to Cause Myositis in a Treg Cell–Deficient Milieu [PDF]
Nicholas A. Young +5 more
openalex +1 more source
This study demonstrates that dual UCP2/IL‐17 blockade reprograms T‐cell metabolism to overcome PDAC immunosuppression. Genipin‐mediated UCP2 inhibition enhances CD8⁺ T‐cell IFN‐γ via IL‐12R/STAT4/mTOR signaling and mitochondrial OXPHOS. Combined IL‐17 depletion amplifies Tc1/Th1 responses, reduces MDSCs, and prolongs survival in PDAC models ...
Chuan‐Teng Liu +11 more
wiley +1 more source
Lei et al. demonstrate that cancer stem cells (CSCs) play a pivotal role in impairing the differentiation of CD103+ T cells in patients with non‐small‐cell lung cancer. The key mechanism involves CSC‐derived acetyl‐CoA, which disrupts CD103+ T cell differentiation by sequentially inducing acetylation and ubiquitination of the Blimp‐1 protein. Targeting
Jiaxin Lei +10 more
wiley +1 more source

