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mRNA Lipid Nanoparticles for Ex Vivo Engineering of Immunosuppressive T Cells for Autoimmunity Therapies

[Nano Letters] Researchers successfully engineered CD4+ T cells into Foxp3-T cells that transiently exhibited an immunosuppressive phenotype and functionally suppressed the proliferation of effector T cells

IL-1β+ Macrophages Fuel Pathogenic Inflammation in Pancreatic Cancer

[Nature] Investigators uncovered an inflammatory loop between tumour cells and interleukin-1β-expressing tumor-associated macrophages, a subset of macrophages elicited by a local synergy between prostaglandin E2, and tumor necrosis factor.

Single-Cell Characterization of Macrophages in Uveal Melanoma Uncovers Transcriptionally Heterogeneous Subsets Conferring Poor Prognosis and Aggressive Behavior

[Experimental & Molecular Medicine] Scientists found that MΦ-C4 exhibited relatively low expression of both M1 and M2 signature genes, loss of inflammatory pathways and antigen presentation, instead demonstrating enhanced signaling for proliferation, mitochondrial functions, and metabolism.

Development of Functional Resident Macrophages in Human Pluripotent Stem Cell-Derived Colonic Organoids and Human Fetal Colon

[Cell Stem Cell] The authors described that pluripotent stem cell-derived human colonic organoids co-developped a diverse population of immune cells, including those that undergo stereotypical steps in differentiation, resulting in the generation of functional macrophages.

Chimeric Autoantibody Receptor T Cells Deplete NMDA Receptor-Specific B Cells

[Cell] Anti-NMDA receptor (NMDAR)-specific chimeric autoantibody receptor T cells recognized a large panel of human patient-derived autoantibodies, released effector molecules, proliferated, and selectively killed antigen-specific target cell lines even in the presence of high autoantibody concentrations.

DOK3 Promotes Atopic Dermatitis by Enabling the Phosphatase PP4C to Inhibit the T Cell Signaling Mediator CARD11

[Science Signaling] Knocking out Dok3 enhanced the production of the cytokine IFN-γ by T cells, which conferred protection against experimental atopic dermatitis–like skin inflammation in mice.

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