G-CSF is an essential regulator of neutrophil trafficking from the bone marrow to the blood

Craig L. Semerad; Fulu Liu; Alyssa D. Gregory; Katherine Stumpf; Daniel C. Link

doi:10.1016/S1074-7613(02)00424-7

G-CSF is an essential regulator of neutrophil trafficking from the bone marrow to the blood

Craig L. Semerad, Fulu Liu, Alyssa D. Gregory, Katherine Stumpf, Daniel C. Link

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358 Scopus citations

Abstract

Neutrophils are released from the bone marrow in a regulated fashion to maintain homeostatic levels in the blood and to respond to physiological stresses, including infection. We show that under basal conditions granulocyte colony-stimulating factor (G-CSF) is an essential regulator of neutrophil release from the bone marrow. Nonredundant signals generated by the membrane-proximal 87 amino acids of the G-CSF receptor (G-CSFR) are sufficient to mediate this response. Surprisingly, G-CSFR expression on neutrophils is neither necessary nor sufficient for their mobilization from the bone marrow, suggesting that G-CSF induces neutrophil mobilization indirectly through the generation of trans-acting signals. Evidence is provided suggesting that downregulation of stromal cell-derived factor 1 expression in the bone marrow may represent such a signal.

Original language	English
Pages (from-to)	413-423
Number of pages	11
Journal	Immunity
Volume	17
Issue number	4
DOIs	https://doi.org/10.1016/S1074-7613(02)00424-7
State	Published - Oct 1 2002

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title = "G-CSF is an essential regulator of neutrophil trafficking from the bone marrow to the blood",

abstract = "Neutrophils are released from the bone marrow in a regulated fashion to maintain homeostatic levels in the blood and to respond to physiological stresses, including infection. We show that under basal conditions granulocyte colony-stimulating factor (G-CSF) is an essential regulator of neutrophil release from the bone marrow. Nonredundant signals generated by the membrane-proximal 87 amino acids of the G-CSF receptor (G-CSFR) are sufficient to mediate this response. Surprisingly, G-CSFR expression on neutrophils is neither necessary nor sufficient for their mobilization from the bone marrow, suggesting that G-CSF induces neutrophil mobilization indirectly through the generation of trans-acting signals. Evidence is provided suggesting that downregulation of stromal cell-derived factor 1 expression in the bone marrow may represent such a signal.",

author = "Semerad, {Craig L.} and Fulu Liu and Gregory, {Alyssa D.} and Katherine Stumpf and Link, {Daniel C.}",

note = "Funding Information: The authors thank Jill Mayer and Morgan McLemore for their expert technical assistance and helpful discussions. This work was supported by a grant from the National Institutes of Health NHLBI (R01 HL60772-01A1; D.C.L.) and by a training grant from the NIH NHLBI (T32 HL 07088-23; C.L.S.). ",

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T1 - G-CSF is an essential regulator of neutrophil trafficking from the bone marrow to the blood

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AU - Liu, Fulu

AU - Gregory, Alyssa D.

AU - Stumpf, Katherine

AU - Link, Daniel C.

N1 - Funding Information: The authors thank Jill Mayer and Morgan McLemore for their expert technical assistance and helpful discussions. This work was supported by a grant from the National Institutes of Health NHLBI (R01 HL60772-01A1; D.C.L.) and by a training grant from the NIH NHLBI (T32 HL 07088-23; C.L.S.).

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N2 - Neutrophils are released from the bone marrow in a regulated fashion to maintain homeostatic levels in the blood and to respond to physiological stresses, including infection. We show that under basal conditions granulocyte colony-stimulating factor (G-CSF) is an essential regulator of neutrophil release from the bone marrow. Nonredundant signals generated by the membrane-proximal 87 amino acids of the G-CSF receptor (G-CSFR) are sufficient to mediate this response. Surprisingly, G-CSFR expression on neutrophils is neither necessary nor sufficient for their mobilization from the bone marrow, suggesting that G-CSF induces neutrophil mobilization indirectly through the generation of trans-acting signals. Evidence is provided suggesting that downregulation of stromal cell-derived factor 1 expression in the bone marrow may represent such a signal.

AB - Neutrophils are released from the bone marrow in a regulated fashion to maintain homeostatic levels in the blood and to respond to physiological stresses, including infection. We show that under basal conditions granulocyte colony-stimulating factor (G-CSF) is an essential regulator of neutrophil release from the bone marrow. Nonredundant signals generated by the membrane-proximal 87 amino acids of the G-CSF receptor (G-CSFR) are sufficient to mediate this response. Surprisingly, G-CSFR expression on neutrophils is neither necessary nor sufficient for their mobilization from the bone marrow, suggesting that G-CSF induces neutrophil mobilization indirectly through the generation of trans-acting signals. Evidence is provided suggesting that downregulation of stromal cell-derived factor 1 expression in the bone marrow may represent such a signal.

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JO - Immunity

JF - Immunity

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ER -

G-CSF is an essential regulator of neutrophil trafficking from the bone marrow to the blood

Abstract

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