Results 121 to 130 of about 552,068 (289)
Pre‐Encoded IFN‐I Sensitivity Exacerbates Memory T Cell Senescence in Solid Tumors
Type I interferon (IFN‐I) signaling promotes p21‐dependent cell cycle arrest in senescent tumor‐specific memory T cells, resulting in poor proliferative responses and solid tumor regression during cancer vaccination. Conversely, IFNα/β receptor blockade reinvigorates T cell proliferation to regress solid tumors and is more effective with increasing ...
Andrew Nguyen +4 more
wiley +1 more source
This study describes a T cell surface engineering strategy that integrates polymer materials with tumor immunology, aiming to achieve broad‐spectrum anti‐tumor applications of glycopolymer‐engineered T (G‐T) cells via non‐genetic modification. Glycopolymer engineering generally modulates immune‐tumor crosstalk through specific cell‐cell interactions ...
Lihua Yao +8 more
wiley +1 more source
Extracellular vesicle (EV)‐packaged CDC37 are released from TMBhiCTLlo breast cancer cells with high CDC37 expression, and internalized into endo/phagosomes of dendritic cells (DCs). Within these compartments, CDC37 locked HSP90–antigen complex, preventing antigen release into the cytosol.
Ruxin Wang +10 more
wiley +1 more source
47 Tertiary lymphoid structures (TLS) in desmoplastic melanomas (DM) differ from non-DM-associated TLS by their intratumoral location and enhanced immune activity [PDF]
Ileana S. Mauldin +10 more
openalex +1 more source
PD‐1 Inhibits CD4+ TRM‐Mediated cDC1 Mobilization via Suppressing JAML in Human NSCLC
CD4+ tissue‐resident memory T cells (TRMs) in non‐small cell lung cancer recruit conventional type 1 dendritic cells via XCL1‐XCR1 signaling, orchestrating antitumor immunity. The costimulatory molecule JAML is essential for this process. PD‐1 blockade restores JAML expression and cDC1 mobilization, while JAML agonists synergize with anti‐PD‐1 therapy,
Zheyu Shao +16 more
wiley +1 more source
Immune checkpoint inhibitors (ICIs) have transformed cancer treatment, providing significant benefit to patients across various tumour types, including melanoma.
Su Yin Lim +9 more
doaj +1 more source
A proposed mechanism to explain the role of CYP4X1/sEH‐14,15‐EET‐EA system in colon cancer immune escape. 14,15‐EET‐EA, 14,15‐epoxyeicosatrienoic acid‐ethanolamide; sEH, soluble epoxide hydrolase; CYP4X1, cytochrome P450 4X1; GPR119, G‐protein coupled receptor 119; EGFR, epidermal growth factor receptor; Gs, Gαs subunit; cAMP, cyclic adenosine ...
Min Mo +10 more
wiley +1 more source
Daniel G, Coit +22 more
openaire +2 more sources

