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Research Article Free access | 10.1172/JCI115543

Interferon-alpha restores the deficient expression of the cytoadhesion molecule lymphocyte function antigen-3 by chronic myelogenous leukemia progenitor cells.

G Upadhyaya, S C Guba, S A Sih, A P Feinberg, M Talpaz, H M Kantarjian, A B Deisseroth, and S G Emerson

Department of Internal Medicine, University of Michigan, Ann Arbor 48109.

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Department of Internal Medicine, University of Michigan, Ann Arbor 48109.

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Department of Internal Medicine, University of Michigan, Ann Arbor 48109.

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Department of Internal Medicine, University of Michigan, Ann Arbor 48109.

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Department of Internal Medicine, University of Michigan, Ann Arbor 48109.

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Department of Internal Medicine, University of Michigan, Ann Arbor 48109.

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Department of Internal Medicine, University of Michigan, Ann Arbor 48109.

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Department of Internal Medicine, University of Michigan, Ann Arbor 48109.

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Published December 1, 1991 - More info

Published in Volume 88, Issue 6 on December 1, 1991
J Clin Invest. 1991;88(6):2131–2136. https://doi.org/10.1172/JCI115543.
© 1991 The American Society for Clinical Investigation
Published December 1, 1991 - Version history
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Abstract

Hematopoietic cells from the malignant clone in chronic myelogenous leukemia (CML) maintain and expand a proliferative advantage over normal hematopoietic cells within the bone marrow. This advantage is often ameliorated or reversed in vivo by IFN alpha. Based upon earlier studies suggesting decreased adhesiveness of CML progenitor cells, we asked whether CML progenitor cells are deficient in their expression of the cytoadhesion molecule lymphocyte function antigen-3 (LFA-3, CD58) which is normally expressed on hematopoietic progenitors. Progenitor cells from untreated CML patients showed greatly reduced or absent LFA-3 expression, whereas progenitors from patients treated with IFN alpha in vivo or in vitro expressed surface LFA-3 at more normal levels. LFA-3-deficient CML progenitor cells were unable to stimulate normal regulatory proliferative responses in autologous T cells. We hypothesize that IFN alpha-sensitive LFA-3 deficiency reflects a cell surface cytoadhesion defect which may help explain adhesive abnormalities of CML progenitor cells in vitro and clonal proliferation in vivo.

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