Results 131 to 140 of about 499,185 (263)

Targeting Peptostreptococcus anaerobius with an Iron‐Based Nanozyme Reverses Ferroptosis Resistance and Enhances Antitumor Immunity in Colorectal Cancer

open access: yesAdvanced Science, EarlyView.
An iron‐based nanozyme selectively eliminates intratumoral P. anaerobius while catalytically generating ROS to induce ferroptosis, synergistically suppressing colorectal cancer growth and activating anti‐tumor immunity through immunogenic cell death. ABSTRACT The intratumoral microbiota is a critical determinant of therapeutic outcomes in colorectal ...
Yinghao Cao   +11 more
wiley   +1 more source

Cytotoxic CD4 T Cells: Dual Agents in HIV-1 Pathogenesis and Persistence. [PDF]

open access: yesCurr HIV/AIDS Rep
Mickens KL   +4 more
europepmc   +1 more source

Oral Streptococcus salivarius Couples Neutrophil IRGM1 Signaling to NET Formation and Colorectal Cancer Metastasis

open access: yesAdvanced Science, EarlyView.
The oral bacterium Streptococcus salivarius promotes colorectal cancer metastasis by inducing neutrophil extracellular trap (NET) formation. Mechanistically, IRGM1–IQGAP1 interaction activates Wnt5a–PI3K/AKT signaling in neutrophils, driving NET‐mediated tumor progression.
Fengyi Liu   +13 more
wiley   +1 more source

SLC2A3‐Mediated Lactate Metabolism Promotes Lung Cancer Bone Metastasis by Modulating P53 Lactylation and Immune Evasion

open access: yesAdvanced Science, EarlyView.
SLC2A3 derived lactate promotes metastasis through p53 lactylation at K120 and osteoclast differentiation. Pharmacological inhibition of SLC2A3 upregulates PD‐1 expression on CD8+ T cells via lactate induced p53 lactylation, which modulates immune evasion. ABSTRACT Bone metastasis is a devastating consequence of lung cancer.
Yi Ding   +10 more
wiley   +1 more source

CD4+ T Cells Mediate MHC-Deficient Tumor Rejection and Endothelial Cell Reprogramming. [PDF]

open access: yesCancer Immunol Res
Kim SI   +12 more
europepmc   +1 more source

Highly Active Cu14 Cluster Precisely Activates Autophagy Inhibitor to Amplify Cuproptosis Immunotherapy

open access: yesAdvanced Science, EarlyView.
An atomically precise Cu14 cluster‐mediated bond scission reaction pioneers the amplification of the antitumor immune response via synergetic cuproptosis‐associated immunogenic cell death induction and in situ autophagy blockade. ABSTRACT Transition metal‐mediated cleavage mechanisms have emerged as an effective means to mitigate the off‐target ...
Qiu‐Xu Zang   +8 more
wiley   +1 more source

Cytotoxic CD4+ T cells in cancer: an emerging target for next-generation anticancer immunotherapy? [PDF]

open access: yesJ Immunother Cancer
van Wandeloo IMB   +4 more
europepmc   +1 more source

Depletion of the RNA‐Editing Enzyme ADAR1 Invigorates the Antitumor Immunity of NK Cells

open access: yesAdvanced Science, EarlyView.
ADAR1 is upregulated in NK cells from melanoma patients, impairing their function. Its loss enhances NK cell tumor infiltration and cytotoxicity in vitro and in vivo. Mechanistically, ADAR1 deficiency destabilizes CD38 mRNA to reduce its expression, thereby increasing NK cell mobility and killing, which nominates it as a therapeutic target for NK cell ...
Shuhan Chen   +11 more
wiley   +1 more source

Peptide-driven identification of TCRs reveals dynamics and phenotypes of CD4 T cells in tuberculosis. [PDF]

open access: yesJ Immunol
Tippalagama R   +16 more
europepmc   +1 more source

Beyond CD30: Dual‐Targeting of Malignant and Regulatory T Cells by Brentuximab Vedotin Remodels the Lymphoma Microenvironment and Overcomes Resistance via BCL2 Inhibition in Mycosis Fungoides

open access: yesAdvanced Science, EarlyView.
Single‐cell RNA analyses of paired lesions from CD30+ mycosis fungoides patients demonstrate that brentuximab vedotin (BV) induces immunogenic cell death in both CD30+ and CD30− malignant T cells. BV also targets regulatory T cells and remodels tumor microenvironment, while resistance is driven by impaired IFN responses, drug efflux, and BCL2 ...
Yi Jiang   +8 more
wiley   +1 more source

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