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Lack of CD47 on nonhematopoietic cells induces split macrophage tolerance to CD47null cells

Hui Wang1, Maria Lucia Madariaga, Shumei Wang

  • 1Transplantation Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02129, USA.

Proceedings of the National Academy of Sciences of the United States of America
|August 19, 2007
PubMed

Insights

Nonhematopoietic cells educate macrophages to recognize and phagocytose CD47-deficient cells. This study reveals a novel mechanism of macrophage tolerance, highlighting the role of nonhematopoietic cells in regulating immune responses.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Macrophages utilize CD47 as a 'self' marker to distinguish and phagocytose cells lacking this protein.
  • Previous understanding suggested CD47's role was primarily cell-autonomous in regulating phagocytosis.

Purpose of the Study:

  • To investigate the role of nonhematopoietic cells in educating macrophages regarding CD47 expression.
  • To elucidate the mechanism by which macrophages develop tolerance to CD47-null cells.

Main Methods:

  • Construction and analysis of CD47 chimera models.
  • Assessment of macrophage phagocytic activity against CD47-null cells in varying chimera configurations.
  • Evaluation of macrophage tolerance to CD47-null red blood cells (RBCs).

Main Results:

  • CD47 expression on nonhematopoietic cells conferred macrophage phagocytic activity against CD47-null hematopoietic cells.
  • Macrophages in chimeras lacking nonhematopoietic CD47 showed tolerance to CD47-null cells.
  • A split tolerance was observed, with macrophages retaining phagocytic activity against CD47-null RBCs.

Conclusions:

  • Nonhematopoietic cells play a critical role in regulating macrophage function and immune tolerance.
  • A novel, previously uncharacterized mechanism of macrophage tolerance mediated by nonhematopoietic cells was identified.
  • These findings suggest potential therapeutic targets for modulating macrophage activity in disease.

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