rebekkaschneider.bsky.social
physician-scientist passionate about research on #MDS, #MPNsm, #fibrosis; CKD; #bonemarrowniche. #oncode; #ERCStg/COG/PoC; twin mom
👤 Joined on 20 November 2024
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@rebekkaschneider.bsky.social7/11 The key message: the spleen is not simply reacting to disease elsewhere. It is an active disease niche, and its local microenvironment may offer new therapeutic opportunities in myelofibrosis.
Show Post6/11 This led us to the complement pathway: and particularly C3 as a potential therapeutic target. Targeting C3 reduced splenomegaly, restored splenic architecture, dampened inflammatory and fibrotic programs, and even reduced bone marrow fibrosis.
Show Post5/11 Reticular stromal cells are central to this process. Initially, they support extramedullary hematopoiesis. As the disease progresses, they shift toward inflammatory and pro-fibrotic states while normal splenic architecture is progressively lost.
Show Post4/11 We found that the spleen is not merely a passive consequence of bone marrow failure. During myelofibrosis, its local microenvironment is actively and progressively remodeled, becoming an integral part of the disease.
Show Post3/11 The project later grew into a wonderful collaboration with @rebekkaschneider.bsky.social, Pia Wanner, and the Aachen team. We combined rare human splenectomy samples, complementary mouse models, and spatial and single-cell technologies.
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