Backgrounds: Chimeric antigen receptor (CAR) T cell therapy has recently exhibited promise as cancer treatment, especiallyfor hematologic malignancies. Currently, all of the FDA-approved CAR T therapies are autologous in nature. This presentsas a limitation since generating CAR T cell using the patient’s own blood leads to higher costs and a 3–4 week productiontime. To overcome this, allogeneic CAR T cell-therapy is being explored.
Objective: In this study, CD45RA depletion was used to generate allogeneic anti-BCMA CAR TT cells. This approach aimsto utilize the CD45RA-negative fraction containing memory T cells which has lower alloreactivity and reduced risk to causegraft-versus-host disease (GVHD).
Methods: The CD45RA-negative T cells were obtained through magnetic separation of CD45RA-labeled PBMCs. Thisprocess yielded the flow-through containing the unlabeled CD45RA-negative fraction which was then used to produceCAR T cells through lentiviral transduction. The generated CD45RA-negative anti-BCMA CAR T cells were compared tonondepleted anti-BCMA CAR T cells according to transduction efficiency, cell expansion, memory phenotype and cellsubset. Cytotoxic function was also assessed through co-culture assays.
Results: Results show higher transduction efficiency and MFI of CD45RA-negative CAR T cells on days 4 and 11,respectively with no difference in expansion. They also feature more CD4+ cell subset and Tem memory phenotype.
Results show no statistically significant difference between non-depleted and depleted anti-BCMA CAR T cells in in vitroco-culture assay.
Conclusion: The data demonstrate CD45RA depletion as a feasible approach to generating allogeneic anti-BCMA CART cells.
Arianwen Rollan, Koramit Suppipa, S. Tawinwung et al.· Journal of Medical Bioscienc...· 0 citations
High-throughput single-cell omics of non-human primate brain tissue provides a powerful platform to investigate the molecular basis of brain aging. Here, we present a comprehensive transcriptomic and chromatin accessibility atlas of 2,955,873 nuclei from eight brain regions of 23 female cynomolgus macaques spanning the adult lifespan, including exceptionally old individuals. Our analyses reveal dynamic, cell-subtype- and region-specific age-related changes in core brain functions, including synaptic communication and axon myelination. We identify multicellular networks in the pons and medulla as a previously unrecognized hotspot of primate brain aging, highlighting white matter vulnerability as a central feature of aging. Integration with human brain aging and neurodegeneration datasets reveals both shared and divergent molecular mechanisms. We further define transcription factors and age-related chromatin remodeling programs linked to longevity and neurodegeneration. This spatiotemporal atlas establishes a foundational framework for understanding the cellular and regulatory architecture of primate brain aging and its links to disease.