Publications by authors named "Yann Pretemer"
Age-associated differences in the effect of repetitive vaccination, particularly on memory T-cell and B-cell responses, remain unclear. While older adults (aged ≥65 years) exhibited enhanced IgG responses following COVID-19 mRNA booster vaccination, they produced fewer spike-specific circulating follicular helper T cells-1 than younger adults. Similarly, the cytotoxic CD8 T-cell response remained diminished with reduced PD-1 expression even after booster vaccination compared with that in younger adults, suggesting impaired memory T-cell activation in older adults.
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- - Camurati-Engelmann disease (CED) is a genetic bone disorder categorized into two types based on TGFB1 mutations, where CED2 lacks these mutations.
- - In this study, researchers discovered two new mutations in the TGFB2 gene in CED2 patients, which affect a specific region of the gene, potentially leading to increased TGF-β2 activity and bone formation.
- - The findings indicate that CED2 may result from heightened TGF-β2 signaling due to a loss of regulatory functions of the latency-associated peptide (LAP), highlighting distinct roles of TGFB1 and TGFB2 in bone development.
Programmable liquid handling devices for cell culture systems have dramatically enhanced scalability and reproducibility. We previously reported a protocol to produce cell aggregates demonstrating growth plate-like structures containing hypertrophic chondrocytes from human induced pluripotent stem cells (hiPSCs). To apply this protocol to large-scale drug screening for growth plate-related diseases, we adapted it to the automated cell culture system (ACCS) consisting of programmable liquid handling devices connected to CO incubators, a refrigerator, and labware feeders, designed for up to 4 batches with several cell culture plates culturing for several months.
View Article and Find Full Text PDFChondrodysplasias are hereditary diseases caused by mutations in the components of growth cartilage. Although the unfolded protein response (UPR) has been identified as a key disease mechanism in mouse models, no suitable in vitro system has been reported to analyze the pathology in humans. Here, we developed a three-dimensional culture protocol to differentiate hypertrophic chondrocytes from induced pluripotent stem cells (iPSCs) and examine the phenotype caused by MATN3 and COL10A1 mutations.
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