Results 71 to 80 of about 119,169 (307)
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
Proteogenomic characterization of cholangiocarcinoma
Proteogenomic characterization of cholangiocarcinoma with therapeutic strategies Abstract Background and Aims Cholangiocarcinoma (CCA) is a highly heterogeneous cancer with limited understanding and few effective therapeutic approaches. We aimed at providing a proteogenomic CCA characterization to inform biological processes and treatment ...
Mengjie Deng +18 more
wiley +1 more source
An autologous whole‐tumor‐cell vaccine (rWTC‐MBTA) is evaluated in murine CNS lymphoma. Subcutaneous vaccination activates dendritic cells, broadens T‐cell priming, and drives lymphocyte trafficking to brain tumors, producing durable tumor control. Longitudinal bioluminescence and adoptive‐transfer assays verify CNS engagement. Combination with anti‐PD‐
Yaping Zhang +10 more
wiley +1 more source
Potential role of immunotherapy in advanced non-small-cell lung cancer [PDF]
Immuno checkpoint inhibitors have ushered in a new era with respect to the treatment of advanced non-small-cell lung cancer. Many patients are not suitable for treatment with epidermal growth factor receptor tyrosine kinase inhibitors (eg, gefitinib ...
Antoniou, Georgios +4 more
core +3 more sources
Osteosarcoma is the most common primary bone tumor with limited treatment options and a terrible prognosis. This review provides a comprehensive summary of the recent development of osteoimmunomodulatory implants for post‐operative osteosarcoma treatment, of which the potential utility in evoking durable anti‐osteosarcoma immunity and accelerating bone
Yilong Dong +6 more
wiley +1 more source
Rigid, bivalent CTLA-4 binding to CD80 is required to disrupt the cis CD80/PD-L1 interaction
Summary: The CTLA-4 and PD-1 checkpoints control immune responses and are key targets in immunotherapy. Both pathways are connected via a cis interaction between CD80 and PD-L1, the ligands for CTLA-4 and PD-1, respectively. This cis interaction prevents
Maximillian A. Robinson +11 more
doaj +1 more source
Evolving Roles for Targeting CTLA-4 in Cancer Immunotherapy
Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) is a membrane glycoprotein expressed by activated effector T cells (Teffs) and participates in the repression of T cell proliferation, cell cycle progression and cytokine production.
Yinghao Zhao +5 more
doaj +1 more source
Expression of CTLA‐4 by Human Monocytes [PDF]
Cytotoxic T lymphocyte‐associated molecule‐4 (CTLA‐4) is a receptor present on T cells that plays a critical role in the downregulation of antigen‐activated immune responses. CTLA‐4 interacts with the ligands CD80 and CD86 on antigen‐presenting cells (APC), and also directs the assembly of inhibitory signalling complexes that lead to quiescence or ...
X-B, Wang +5 more
openaire +2 more sources
Polymorphism analysis of the CTLA-4 (rs231775) gene as a marker of inhibitor development in Iranian patients with hemophilia A [PDF]
Background: Development of factor VIII (FVIII) inhibitor is the main problem of replacement therapy in patients with hemophilia A. Recently, the correlation of polymorphisms of some genes involved in immune system has been determined with inhibitor ...
Bolhassani, Azam +2 more
core +1 more source
MALT1 proteolytic activity suppresses autoimmunity in a T cell intrinsic manner [PDF]
MALT1 is a central signaling component in innate and adaptive immunity by regulating NF-kappa B and other key signaling pathways in different cell types. Activities of MALT1 are mediated by its scaffold and protease functions.
Baens, Mathijs +7 more
core +2 more sources

