Splenic extramedullary hematopoiesis in myelofibrosis is shaped by transcriptomic and epigenetic dysregulation.
Splenic extramedullary hematopoiesis in myelofibrosis involves significant transcriptomic and epigenetic dysregulation, with expansion of progenitor cells and immune microenvironment remodeling.
- Why it matters: Understanding these molecular mechanisms is crucial because they drive abnormal blood cell production and immune alterations that worsen disease progression and hinder immune responses in myelofibrosis.
- What they did: Single-cell transcriptional and chromatin profiling of MF spleen cells revealed expanded hematopoietic stem and progenitor populations, aberrant differentiation, and immune microenvironment changes involving inflammatory pathways and dysfunctional immune cell subsets.
- The result: These findings highlight how transcriptomic and epigenetic dysregulation shape splenic EMH and immune landscape, providing potential targets for therapies to restore normal hematopoiesis and immune function in myelofibrosis.