Results 101 to 110 of about 333,809 (260)
RGS16 competitively interferes with the YTHDF3–PAN3 complex to prevent CXCL1 mRNA decay during hepatic ischemia‐reperfusion injury. Stabilized CXCL1 strengthens hepatocyte injury, neutrophil recruitment, and NET‐associated inflammation, uncovering how stress‐induced RGS16 converts post‐transcriptional regulation into immune‐mediated liver damage ...
Xinglong Li +16 more
wiley +1 more source
Exposure to CS causes an elevation of AARS1 levels, which increases the levels of RUNX3 lactylation at the K193 site and increases protein levels of RUNX3 through inhibition of autolysosomal degradation. Elevated RUNX3 levels promote CD8+T cell activation and augment their cytotoxicity, which induces alveolar epithelial cell death and facilitates the ...
Ying Zhu +12 more
wiley +1 more source
This work identified CPD3a as a potent, stable C‐nucleoside cordycepin derivative. When formulated into microneedle array for topical treatment, it ameliorated psoriasis by rebalancing immunity and enhancing antioxidant defenses. ABSTRACT Psoriasis is a chronic inflammatory disorder characterized by immune dysregulation and epidermal hyperplasia ...
Wenfang Pan +7 more
wiley +1 more source
Chimeric antigen receptor T-cell therapy for aggressive B-cell lymphomas
Chimeric antigen receptor (CAR) T-cell therapy is a revolutionary approach in the treatment of lymphoma. This review article provides an overview of the four FDA-approved CAR T-cell products for aggressive B-cell lymphoma, including diffuse large B-cell ...
Bei Hu +3 more
doaj +1 more source
Repurposing a Small Molecule Plant Hormone as a Tunable ON‐Switch for CAR‐T Cell Immunotherapy
By engineering a receptor system integrating the plant auxin receptor AFB1 with its co‐receptor IAA7, we enable ligand‐dependent interactions triggered by the plant hormone auxins. This design allows rapid, reversible, and dose‐dependent T cell activation, resulting in potent cytotoxicity against B‐cell lymphoma in vitro and in vivo.
Hongxiang Zeng +16 more
wiley +1 more source
IFI27 and BAX are Essential for GSDME‐Mediated Myeloma Cell Pyroptosis
The proposed model of GSDME‐mediated MM cell pyroptosis modulated by IFI27 and BAX. IFI27 is downregulated in MM cells. Upon pyroptotic stimulation, such as DOX or ETO treatment, IFI27 is induced, therefore liberating BAX from BCL‐2 ❶. BAX is then recruited to mitochondria and forms homo‐oligomeric channels in OMM, therefore leading to cytochrome C ...
Yaoli Cui +12 more
wiley +1 more source
EBV‑BZLF1 initiates ODC1‑driven polyamine anabolism that correlates with poor clinical prognosis in nasopharyngeal carcinoma. The ODC1–spermidine axis promotes viral replication, cell proliferation and innate immune evasion. Pharmacological inhibition of ODC1 rescues cisplatin sensitivity, establishing ODC1 as a viable therapeutic target for EBV ...
Yueshuo Li +9 more
wiley +1 more source
ABSTRACT Memory T cells exhibit long‐term persistence, a defining feature that underpins durable clinical responses to adoptive immunotherapies. The mechanisms that integrate metabolic cues with transcriptional control of memory fate remain undetermined. Here, we identify HS1‐binding protein 3 (HS1BP3) is preferentially expressed in memory CD8+ T cells.
Siyang Wang +13 more
wiley +1 more source
A mechanically activated SynNotch reporter platform enables detection of force transmission through receptors as they mediate immune cell interactions. Targeting CD40 on B cells and TCR on T cells records force‐induced reporter activation across 2D coculture, 3D organoid, and implanted in mice, which also reveal force‐amplification of immune receptor ...
Menglan Li +9 more
wiley +1 more source
In this study, we identify a novel functional role of ZBTB18 in regulating trigeminal‐mediated neuropathic pain. Nerve injury reduces ZBTB18 in trigeminal ganglion neurons, impairing CHD4/NuRD recruitment and de‐repressing Clic1. Elevated CLIC1 enhances chloride channel activity and neuronal hyperexcitability, thereby driving pain.
Shoupeng Wang +11 more
wiley +1 more source

