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Research Article Free access | 10.1172/JCI118141

Treatment of marrow stroma with interferon-alpha restores normal beta 1 integrin-dependent adhesion of chronic myelogenous leukemia hematopoietic progenitors. Role of MIP-1 alpha.

R Bhatia, P B McGlave, and C M Verfaillie

Department of Medicine, University of Minnesota, Minneapolis 55455, USA.

Find articles by Bhatia, R. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Minnesota, Minneapolis 55455, USA.

Find articles by McGlave, P. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Minnesota, Minneapolis 55455, USA.

Find articles by Verfaillie, C. in: JCI | PubMed | Google Scholar

Published August 1, 1995 - More info

Published in Volume 96, Issue 2 on August 1, 1995
J Clin Invest. 1995;96(2):931–939. https://doi.org/10.1172/JCI118141.
© 1995 The American Society for Clinical Investigation
Published August 1, 1995 - Version history
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Abstract

The mechanisms by which interferon-alpha (IFN-alpha) restores normal hematopoiesis in chronic myelogenous leukemia (CML) are not well understood. We have recently demonstrated that IFN-alpha acts directly on CML hematopoietic progenitors to restore their adhesion to marrow stroma by modulating beta 1 integrin receptor function. In the present study we examined the effect of IFN-alpha treatment of marrow stroma on subsequent adhesion of CML progenitors. Stromal layers were preincubated with IFN-alpha (10,000 microns/ml) for 48 h. Subsequent coincubation with CML progenitors for 2 h resulted in significantly increased adhesion of CML progenitors. We demonstrated that alpha 4 beta 1 and alpha 5 beta 1 integrin receptors were involved in the enhanced adhesion of CML progenitors, suggesting that IFN-alpha-treated stroma can upregulate CML integrin function. This effect is due, at least in part, to IFN-alpha-induced increased stromal production of the chemokine macrophage inflammatory protein-1 alpha (MIP-1 alpha), which upregulates beta 1 integrin-dependent adhesion of CML progenitors to stroma. Thus, IFN-alpha treatment of marrow stroma restores beta 1 integrin-dependent adhesion of CML progenitors, at least in part through induction of MIP-1 alpha production. These observations provide further insights into mechanisms by which IFN-alpha may restore normal hematopoiesis in CML.

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