Publications by authors named "Cindy Evandy"
Article Synopsis
- Endogenous thymic regeneration is essential for the immune system's recovery after stress, infection, or damage, and understanding how this process works can lead to new therapies.
- The study found that high apoptosis levels hinder regeneration, while reducing damaged apoptotic thymocytes can promote it, and that metabolic changes in thymocytes post-radiation lead to a specific type of cell death.
- A key molecule, ATP, activates the P2Y2 receptor on thymic epithelial cells, enhancing a transcription factor vital for thymus function; targeting this receptor can enhance thymus regeneration after damage.
Prolonged lymphopenia represents a major clinical problem after cytoreductive therapies such as chemotherapy and the conditioning required for hematopoietic stem cell transplant (HCT), contributing to the risk of infections and malignant relapse. Restoration of T-cell immunity depends on tissue regeneration in the thymus, the primary site of T-cell development, although the capacity of the thymus to repair itself diminishes over its lifespan. However, although boosting thymic function and T-cell reconstitution is of considerable clinical importance, there are currently no approved therapies for treating lymphopenia.
View Article and Find Full Text PDFThe thymus, which is the primary site of T cell development, is particularly sensitive to insult but also has a remarkable capacity for repair. However, the mechanisms orchestrating regeneration are poorly understood, and delayed repair is common after cytoreductive therapies. Here, we demonstrate a trigger of thymic regeneration, centered on detecting the loss of dying thymocytes that are abundant during steady-state T cell development.
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