Results 171 to 180 of about 574,897 (264)

CCL3 and IL‐7 Synergistically Enhance CAR‐T Efficacy in Solid Tumors

open access: yesAdvanced Science, EarlyView.
Synergistic delivery of CCL3 and IL‐7 by CAR‐T cells overcomes the immunosuppressive tumor microenvironment by enhancing cell infiltration, survival, and local immune reprogramming. This also establishes positive feedback that amplifies anti‐tumor activity and memory responses in both CAR‐T and endogenous T cells, presenting a robust therapeutic ...
Huanpeng Chen   +12 more
wiley   +1 more source

Role of CD4+ T Cells and of the CD4 Molecule in Contact Sensitivity

open access: yesJournal of Investigative Dermatology, 1997
Bour, Hélène   +3 more
openaire   +2 more sources

Tumor‐Specific Delivery of CD28 siRNA via Lyso‐PC C‐16 Modified Lipid Nanoparticles Overcomes Anti‐PD‐1 Resistance by Remodeling Tumor Microenvironment

open access: yesAdvanced Science, EarlyView.
This study develops 16:0 LPC‐modified lipid nanoparticles (LPC‐LNPs) with cancer cell specificity by exploiting altered tumor lipid metabolism. LPC‐LNPs encapsulating Cd28 small interfering RNA (LPC‐LNP‐Cd28) knock down cancer cell CD28 without affecting T cells, inflame the tumor microenvironment, and overcome anti‐PD‐1 resistance.
Yangyang Chai   +12 more
wiley   +1 more source

Targeting Lactate‐Driven Stromal Autophagy via MCT1 Disrupts the Immunosuppressive Niche and Sensitizes Pancreatic Cancer to PD‐1 Blockade

open access: yesAdvanced Science, EarlyView.
Tumor‐derived lactate activates PSCs through MCT1‐mediated Vps34 lactylation and autophagy. These activated PSCs secrete CXCL9/10, upregulating PD‐1 on CD8+ T cells via the CXCR3/STAT3 axis to foster immunosuppression. Disrupting this metabolic crosstalk by targeting MCT1 effectively sensitizes pancreatic cancer to PD‐1 blockade, presenting a promising
Wenfeng Zhuo   +14 more
wiley   +1 more source

Allosteric Inhibition of Polycomb Repressive Complex 2 by an EZH2‐Selective Small Molecule Inhibitor

open access: yesAdvanced Science, EarlyView.
The study characterizes C36, a highly selective EZH2/PRC2 inhibitor that acts via a novel allosteric mechanism. Unlike previous inhibitors, C36 inhibits EZH2/PRC2 by disrupting the allosteric communication between EZH2 and EED in a SAM‐noncompetitive manner.
Ting Cao   +11 more
wiley   +1 more source

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