期刊
IMMUNITY
卷 25, 期 6, 页码 895-906出版社
CELL PRESS
DOI: 10.1016/j.immuni.2006.10.013
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-
类别
资金
- NHLBI NIH HHS [HL56385, HL53949, HL64353, HL66600] Funding Source: Medline
The integrin alpha 9 beta 1 is widely expressed on neutrophils, smooth muscle, hepatocytes, endothelia, and some epithelia. We now show that mice lacking this integrin have a dramatic defect in neutrophil development, with decreased numbers of granulocyte precursors in bone marrow and impaired differentiation of bone marrow cells into granulocytes. In response to granulocyte colony-stimulating factor (G-CSF), alpha 9-deficient bone marrow cells or human bone marrow cells incubated with alpha 9 beta 1-locking antibody demonstrated decreased phosphorylation of signal transducer and activator of transcription 3 and extracellular signal-regulated protein kinase. These effects depended on the alpha 9 subunit cytoplasmic domain, which was required for formation of a physical complex between alpha 9 beta 1 and ligated G-CSF receptor. Integrin alpha 9 beta 1 was required for granulopoiesis and played a permissive role in the G-CSF-signaling pathway, suggesting that this integrin could play an important role in disorders of granulocyte development and other conditions characterized by defective G-CSF signaling.
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