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, S. G. Emerson

Research output: Contribution to journalArticlepeer-review

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(α). 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(α) 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(α)-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.

Original languageEnglish (US)
Pages (from-to)2131-2136
Number of pages6
JournalJournal of Clinical Investigation
Volume88
Issue number6
DOIs
StatePublished - 1991
Externally publishedYes

Keywords

  • Adhesion
  • Clonal expansion
  • Stem cell

ASJC Scopus subject areas

  • Medicine(all)

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