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Expression of intercellular adhesion molecule-1 (CD54) on hematopoietic progenitors

S Arkin1, B Naprstek, L Guarini

  • 1Division of Pediatric Hematology-Oncology, Mount Sinai School of Medicine, New York, NY 10029.

Blood
|March 1, 1991
PubMed

Insights

Intercellular adhesion molecule-1 (ICAM-1) is present on early hematopoietic progenitors but diminishes as cells mature. This suggests ICAM-1 plays a role in regulating blood cell formation and interactions.

Area of Science:

  • Hematology
  • Immunology
  • Cell Biology

Background:

  • Intercellular adhesion molecule-1 (ICAM-1) is a key molecule involved in cell-cell interactions.
  • Its distribution on hematopoietic cells is not fully understood, particularly in relation to progenitor cells and maturation.
  • Previous reports have varied regarding ICAM-1 expression on hematopoietic cells.

Purpose of the Study:

  • To determine the distribution of ICAM-1 on hematopoietic progenitor cells and differentiating myeloid and erythroid lineages.
  • To investigate the potential role of ICAM-1 in regulating hematopoiesis.

Main Methods:

  • Utilized anti-ICAM-1 monoclonal antibody CL203.4 for detection.
  • Employed flow cytometry to analyze ICAM-1 expression.
  • Used short-term semi-solid hematopoietic progenitor cultures.

Main Results:

  • ICAM-1 was expressed on a significant percentage of erythroid burst-forming units (BFU-E), erythroid colony-forming units (CFU-E), and granulocyte-macrophage colony-forming units (CFU-GM).
  • Expression was also found on bone marrow blasts, proerythroblasts, promyelocytes, and monocyte/macrophage lineage cells.
  • ICAM-1 was notably absent on more mature erythroid cells (erythroblasts, normoblasts) and myeloid cells (myelocytes, bands), indicating loss during maturation.

Conclusions:

  • Hematopoietic progenitor cells and early precursor cells express ICAM-1.
  • Maturation of erythroid and myeloid lineages is associated with a loss of ICAM-1 expression.
  • ICAM-1 likely contributes to the cell-cell and cell-stromal interactions essential for regulating hematopoiesis.

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