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Engineered IL-7 Synergizes with IL-12 Immunotherapy to Prevent T Cell Exhaustion and Promote Memory without Exacerbating Toxicity

[Science Advances] Scientists showed that the combination of engineered, tumor matrix-binding IL-7 and IL-12 achieves remarkable anticancer effects by activating complementary pathways without inducing any additive immunotoxicity.

Unrestrained Cleavage of Roquin-1 by MALT1 Induces Spontaneous T Cell Activation and the Development of Autoimmunity

[Proceedings Of The National Academy Of Sciences Of The United States Of America] Investigators showed that autoimmunity, caused by conventional T cells expressing constitutively active MALT1 paracaspase, was triggered by cleavage of a single substrate, the RNA-binding protein Roquin-1.

Ginseng-Derived Nanoparticles Reprogram Macrophages to Regulate Arginase-1 Release for Ameliorating T Cell Exhaustion in Tumor Microenvironment

[Journal of Experimental & Clinical Cancer Research] By regulating the mTOR-T-bet axis, ginseng-derived nanoparticles reprogramed macrophages to regulate arginase-1 release, which further ameliorated T cell exhaustion in tumor microenvironment.

MDSCs-Derived GPR84 Induces CD8+ T Cell Senescence via p53 Activation to Suppress the Antitumor Response

[Journal for Immunotherapy of Cancer] Scientists showed that the transfer of G-protein-coupled receptor 84 (GPR84) from myeloid-derived suppressor cells (MDSCs) to CD8+ T cells via the exosomes attenuated the antitumor response.

PD-1 Inhibits T Cell Actin Remodeling at the Immunological Synapse Independently of Its Signaling Motifs

[Science Signaling] Researchers investigated the mechanisms underlying programmed cell death molecule 1 (PD-1)–mediated inhibition. Their findings suggest an alternative mechanism by which PD-1 regulated immune responses.

METTL3 Promotes Colorectal Cancer Progression through Activating JAK1/STAT3 Signaling Pathway

[Cell Death & Disease] Investigators revealed that upregulated methyltransferase-like 3 (METTL3) in colorectal cancer exerted both methyltransferase activity-dependent and -independent functions in gene regulation.

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