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Summary: Hematopoietic stem cells (HSCs) reside and selfrenew in the Bone marrow (BM) (BM) niche. Overall, the signaling that regulates stem cell dormancy in the HSC niche remains controversial. Here, we demonstrate that TGF-b type II receptor-deficient HSCs show low-level Smad activation and impaired longterm repopulating activity, underlining the critical role of TGF-b/Smad signaling in HSC maintenance. TGF-b is produced as a latent form by a variety of cells, so we searched for those that express activator molecules for latent TGF-b. Nonmyelinating Schwann cells in BM proved responsible for activation. These glial cells ensheathed autonomic nerves, expressed HSC niche facto…