The paper investigates the cellular and molecular mechanisms driving splenomegaly and fibrosis in human and murine myelofibrosis (MF), a chronic myeloproliferative neoplasm. By combining spatial and single-cell transcriptomics with advanced imaging, researchers discovered that reticular cells (RCs) in the splenic stromal niche undergo a pathological shift from supporting hematopoiesis to promoting inflammation and fibrosis as the disease advances. This aberrant remodeling is heavily driven by macrophage-derived signals and complement component C3, which disrupt lymphoid architecture and accelerate disease severity. Crucially, the studies demonstrate that C3 inhibition or deficiency can suppress these profibrotic pathways, restore healthy splenic architecture, and significantly reduce fibrotic progression in both the spleen and bone marrow.
References:
Dugué B, Wanner P, Segura M L R T, et al. Spatial profiling of the spleen in mouse and human myelofibrosis reveals complement-driven immune-stromal interactions as a therapeutic target[J]. Cell Stem Cell, 2026, 33(9): 1477-1494. e14.
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