Engagement of p75/AIRM1 or CD33 inhibits the proliferation of normal or leukemic myeloid cells

Chiara Vitale, Chiara Romagnani, Michela Falco, Marco Ponte, Massimo Vitale, Alessandro Moretta, Andrea Bacigalupo, Lorenzo Moretta, Maria Cristina Mingari

Research output: Contribution to journalArticle

Abstract

P75/AIRM1 is a recently identified surface molecule that belongs to the sialoadhesin family and displays homology with the myeloid cell antigen CD33. In lymphoid cells, p75/AIRM1 is confined to natural killer cells and mediates inhibition of their cytolytic activity. In this study, we show that p75/AIRM1 is also expressed by cells of the myelomonocytic cell lineage, in which it appears at a later stage as compared with CD33. In vitro proliferation and differentiation of cord blood-derived CD34+ cells (induced by stem cell factor and granulocyte-macrophage colony-stimulating factor) were consistently inhibited by the addition of anti-p75/AIRM1 mAb. Engagement of CD33 led to inhibition in some experiments. A sharp decrease of cell proliferation/survival was detected in all three p75/AIRM1+ chronic myeloid leukemias analyzed when cultured in the presence of either anti-p75/AIRM1 or anti-CD33 mAbs. Thus, the present study suggests that p75/AIRM1 and CD33 may play a regulatory role in normal myelopoiesis and may be viewed as suitable target molecules to counteract the proliferation/survival of chronic myeloid leukemias.

Original languageEnglish
Pages (from-to)15091-15096
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume96
Issue number26
DOIs
Publication statusPublished - Dec 21 1999

ASJC Scopus subject areas

  • Genetics
  • General

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