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IL‐1RI‐dependent Hematopoietic Stem Cell Proliferation in Support of Inflammatory Granulopoiesis
Author(s) -
Ueda Yoshihiro,
Cain Derek,
Kondo Motonari,
Kelsoe Garnett
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.844.1
Subject(s) - granulopoiesis , neutrophilia , haematopoiesis , granulocyte , progenitor cell , stem cell , bone marrow , immunology , microbiology and biotechnology , inflammation , granulocyte colony stimulating factor , hematopoietic stem cell , biology , genetics , chemotherapy
Normally, steady‐state granulopoiesis generates adequate numbers of bone marrow (BM) and peripheral neutrophils. Infection and inflammation mobilize these neutrophil pools and trigger a distinct hematopoietic program of increased granulopoiesis necessary to support the reactive neutrophilia elicited by microbial infections. Whereas inflammatory granulopoiesis can be defined by its requirement for the C/EBPbeta transcription factor, the cellular cues that activate this special granulopoietic pathway are unknown. We demonstrate that adjuvant‐induced, reactive neutrophilias are the consequence of IL‐1R signals that induce hematopoietic stem cell (HSC) proliferation and preferential differentiation into granulocyte progenitors. We propose that the switch from steady‐state to inflammatory granulopoiesis occurs prior to granulocyte lineage commitment through IL‐1RI signaling.