Publications by authors named "C Berthault"
Objectives: This study aimed to evaluate the efficacy of a purification method developed for isolating alpha, beta, and delta cells from pancreatic islets of adult mice, extending its application to islets from newborn and aged mice. Furthermore, it sought to examine transcriptome dynamics in mouse pancreatic endocrine islet cells throughout postnatal development and to validate age-related alterations within these cell populations.
Methods: We leveraged the high surface expression of CD71 on beta cells and CD24 on delta cells to FACS-purify alpha, beta, and delta cells from newborn (1-week-old), adult (12-week-old), and old (18-month-old) mice.
Recessive dystrophic epidermolysis bullosa (RDEB) is a rare and severe genetic skin disease responsible for blistering of the skin and mucosa after minor trauma. RDEB is caused by a wide variety of variants in COL7A1 encoding type VII Collagen, the major component of anchoring fibrils that form key attachment structures for dermal-epidermal adherence. In this study, we achieved highly efficient COL7A1 editing in primary RDEB keratinocytes and fibroblasts from 2 patients homozygous for the c.
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- The study investigates how pancreatic β cells can resist immune attacks in type 1 diabetes by lowering HLA class I expression and increasing immune inhibitors like PD-L1.
- Tryptophan (TRP) was found to induce PD-L1 through the AKT signaling pathway, which helps β cells evade immune detection while simultaneously reducing the expression of other immune activators like HLA-I and CXCL10.
- Overall, TRP could promote immune tolerance in β cells, making it a potential therapeutic avenue for managing type 1 diabetes by enhancing immune evasion mechanisms.
Article Synopsis
- * A study using flow cytometry found that alpha and delta cells exposed to IFNγ, a significant cytokine in T1D, show a similar inflammatory response as beta cells, including increased expression of key inflammation-related genes.
- * Researchers discovered that the sensitivity to IFNγ among beta cells varies based on their location within the islet rather than being due to distinct cell types, indicating a gradual spread of the cytokine and enhancing our understanding of the inflammatory dynamics in T1D.
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is involved in the degradation of the low-density lipoprotein receptor. PCSK9 also targets proteins involved in lipid metabolism (very low-density lipoprotein receptor), immunity (major histocompatibility complex I), and viral infection (cluster of differentiation 81). Recent studies have also indicated that PCSK9 loss-of-function mutations are associated with an increased incidence of diabetes; however, the expression and function of PCSK9 in insulin-producing pancreatic beta cells remain unclear.
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