Results 151 to 160 of about 73,275 (286)
HEK‐293T‐derived CD3ε Nb‐engineered EVs to generate dual‐targeting CAR‐T cells directly in vivo. These EVs selectively deliver CAR.BiTE transgenes into T cells and reprogramed to HLA‐G/PD‐L1‐targeting effector cells with enhanced memory and persistence.
Shi‐Wei Huang +27 more
wiley +1 more source
Cellular Identity Crisis: RD3 Loss Fuels Plasticity and Immune Silence in Progressive Neuroblastoma
Researchers discovered that therapy‐induced loss of RD3 protein in neuroblastoma triggers a dangerous shift: cancer cells become more stem‐like, invasive, and resistant to treatment while evading immune detection. RD3 loss suppresses antigen presentation and boosts immune checkpoints, creating an immune‐silent environment.
Poorvi Subramanian +7 more
wiley +1 more source
ZBTB21 is a transcription factor that epigenetically suppresses pyroptosis and MHC‐I antigen presentation, enabling tumor immune evasion. Genetic ablation of ZBTB21 activates pyroptotic cell death and enhances antigen presentation, recruiting CD8+ T cells to overcome immune checkpoint blockade resistance.
Lei Zhao +12 more
wiley +1 more source
We developed a macrophage‐based therapeutic platform, termed trackable tolerogenic macrophages (TTM), for dual‐function immunomodulation and visualization in vivo. TTM cells were engineered to overexpress PD‐L1, incorporate bioorthogonal cell surface tags, and load rapamycin for sustained release.
Yihui Wang +14 more
wiley +1 more source
Regulatory T cells (Tregs) suppress antitumor immunity. This study identifies that the translation scaffold DAP5/eIF4G2 is upregulated in tumor‐infiltrating Tregs (ti‐Tregs). DAP5 mediates an alternate translation mode to sustain CD25 and MCL‐1 expression, which is critical for ti‐Treg stability and survival in the tumor microenvironment.
Xiaojiang Lai +12 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
This study emphasizes the role of the Mapk13‐Tcf1‐Slc7a5‐methionine metabolism axis in stem‐like CD4+ T cells. Moreover, it uncovers the mechanism through which limiting one‐carbon metabolism in CD4+ stem‐like T cells suppresses the tide of chronic allograft vasculopathy, offering potential targets to promote long‐term graft survival.
Wang Yi +8 more
wiley +1 more source
This study uncovers a recipient‐derived monocyte‐to‐macrophage trajectory that drives inflammation during kidney transplant rejection. Using over 150 000 single‐cell profiles and more than 850 biopsies, the authors identify CXCL10+ macrophages as key predictors of graft loss.
Alexis Varin +16 more
wiley +1 more source
Tumor Antigen-reactive CD28 /CCR7 /CD27 /CD45RA- Cytotoxic T-lymphocyte [PDF]
openaire +1 more source
Pro‐Inflammatory c‐Met+ CD4 T Cells in Multiple Sclerosis
Objective Hepatocyte growth factor (HGF) binds exclusively the c‐Met surface receptor, and the HGF/c‐Met axis regulates T cell function in autoimmune diseases. We analyzed c‐Met expression on human CD4 T cells in the blood and cerebrospinal fluid (CSF) from patients with multiple sclerosis (MS) versus non‐inflammatory neurological disease (NIND), to ...
Gautier Breville +6 more
wiley +1 more source

