Advertisement
Research Article Free access | 10.1172/JCI115543
Department of Internal Medicine, University of Michigan, Ann Arbor 48109.
Find articles by Upadhyaya, G. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, University of Michigan, Ann Arbor 48109.
Find articles by Guba, S. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, University of Michigan, Ann Arbor 48109.
Find articles by Sih, S. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, University of Michigan, Ann Arbor 48109.
Find articles by Feinberg, A. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, University of Michigan, Ann Arbor 48109.
Find articles by Talpaz, M. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, University of Michigan, Ann Arbor 48109.
Find articles by Kantarjian, H. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, University of Michigan, Ann Arbor 48109.
Find articles by Deisseroth, A. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, University of Michigan, Ann Arbor 48109.
Find articles by Emerson, S. in: JCI | PubMed | Google Scholar
Published December 1, 1991 - More info
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.
Images.