This study reveals that STAT1 is a critical regulator of hematopoietic stem cell biology, specifically in a subset of HSCs characterized by elevated levels of MHCIIhi. This subset of HSCs possesses resistance against stress-induced myeloablation and is not expanded in calreticulin mutant mice.
In this issue of Blood, Li et al1 add a fresh perspective to our understanding of hematopoietic stem cell (HSC) functions. The authors explain that signal transducer and activator of transcription 1 (STAT1) is a critical steady-state regulator of HSC biology. Specifically, STAT1 is a key regulator of a subset of HSCs characterized by elevated levels of major histocompatibility complex II (MHCIIhi). This MHCIIhi HSC subset resists stress-induced myeloablation and is not expanded in calreticulin mutant (CALR(del/del)) mice (see figure).
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