4 results match your criteria: "Institute of Cell Engineering and.[Affiliation]"
Bone Res
March 2022
Department of Orthopedic Surgery, Institute of Cell Engineering and Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
The molecular control of osteoclast formation is still not clearly elucidated. Here, we show that a process of cell recognition mediated by Siglec15-TLR2 binding is indispensable and occurs prior to cell fusion in RANKL-mediated osteoclastogenesis. Siglec15 has been shown to regulate osteoclastic bone resorption.
View Article and Find Full Text PDFT cell polyfunctionality is a hallmark of protective immunity against pathogens and cancer, yet the molecular mechanism governing it remains mostly elusive. We found that canonical Wnt agonists inhibited human memory CD8+ T cell differentiation while simultaneously promoting the generation of highly polyfunctional cells. Downstream effects of Wnt activation persisted after removal of the drug, and T cells remained polyfunctional following subsequent cell division, indicating the effect is epigenetically regulated.
View Article and Find Full Text PDFOncotarget
August 2018
Institute of Cell Engineering and Department of Pathology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
[This corrects the article DOI: 10.18632/oncotarget.11785.
View Article and Find Full Text PDFOncotarget
October 2016
Institute of Cell Engineering and Department of Pathology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Redirection of T cells to target and destroy tumors has become an important clinical tool and major area of research in tumor immunology. Here we present a novel, nanoparticle-based approach to selectively bind antigen-specific cytotoxic T cells (CTL) and redirect them to kill tumors, termed ATR (Antigen-specific T cell Redirectors). ATR were generated by decorating nanoparticles with both an antigen-specific T cell binding moiety, either peptide loaded MHC-Ig dimer or clonotypic anti-TCR antibody, and a model tumor cell binding moiety, anti-CD19 antibody to engage CD19+ tumor cells.
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