Abstract:
UNLABELLED:Polymorphonuclear neutrophil granulocytes (neutrophils) are tightly controlled by an incompletely understood homeostatic feedback loop adjusting the marrow's supply to peripheral needs. Although it has long been known that marrow cellularity is inversely correlated with G-CSF levels, the mechanism linking peripheral clearance to production remains unknown. Herein, the feedback response to antibody induced neutropenia is characterized to consist of G-CSF–dependent shifts of marrow hematopoietic progenitor populations including expansion of the lin-/Sca-1/c-kit (LSK) and granulocyte macrophage progenitor (GMP) compartments at the expense of thrombopoietic and red cell precursors. Evidence is provided that positive feedback regulation is independent from commensal germs as well as T, B, and NK cells. However, in vivo feedback is impaired in TLR4-/- and TRIF-/-, but not MyD88-/- animals. In conclusion, steady-state neutrophil homeostasis is G-CSF–dependent and regulated through pattern-recognition receptors,thereby directly linking TLR-triggering to granulopoiesis. KEY POINTS:Steady-state and emergency granulopoiesis are both dependent on TLR signaling.
journal_name
Bloodjournal_title
Bloodauthors
Bugl S,Wirths S,Radsak MP,Schild H,Stein P,André MC,Müller MR,Malenke E,Wiesner T,Märklin M,Frick JS,Handgretinger R,Rammensee HG,Kanz L,Kopp HGdoi
10.1182/blood-2012-05-429589subject
Has Abstractpub_date
2013-01-31 00:00:00pages
723-33issue
5eissn
0006-4971issn
1528-0020pii
blood-2012-05-429589journal_volume
121pub_type
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