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Immunobiologic differences between normal and leukemic human B-cell precursors.

F M Uckun1, J A Ledbetter

  • 1Department of Therapeutic Radiology-Radiation Oncology, University of Minnesota, Minneapolis 55455.

Proceedings of the National Academy of Sciences of the United States of America
|November 1, 1988
PubMed
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CD10 expression precedes CD19 expression during normal B-cell development. Leukemic B-cell precursors show altered responses to growth factors and CD19 signaling, suggesting CD19

Area of Science:

  • Immunology
  • Developmental Biology
  • Hematology

Background:

  • Understanding early human B-cell differentiation is crucial for diagnosing and treating B-cell precursor acute lymphoblastic leukemias (ALLs).
  • The roles of CD10 and CD19 cell surface antigens in normal and malignant B-cell development are not fully elucidated.

Purpose of the Study:

  • To investigate the sequential expression of CD10 and CD19 during normal human B-cell ontogeny.
  • To compare the in vitro proliferative responses of normal B-cell precursors with those of leukemic B-cell precursors from ALL patients.
  • To explore the potential involvement of the CD19 receptor in B-cell leukemogenesis.

Main Methods:

  • Flow cytometry and cell sorting were used to isolate and analyze B-cell precursor populations from fetal liver and bone marrow.

Related Experiment Videos

  • In vitro proliferation assays were performed using various B-cell growth factors (L-BCGF, H-BCGF, rIL-3).
  • CD19 crosslinking experiments were conducted to assess its effect on calcium concentration and colony formation.

    • Main Results:

    • CD10 expression appears to precede CD19 expression in normal B-cell ontogeny, as indicated by CD10+CD19- precursor populations.
    • Normal B-cell precursors responded to L-BCGF and rIL-3 but not H-BCGF, and CD19 crosslinking inhibited colony formation.
    • Leukemic B-cell precursors from ALL patients responded to both L-BCGF and H-BCGF, and CD19 crosslinking stimulated their proliferation.
    • A clonogenic leukemic counterpart for the normal CD10+CD19- precursor population was not identified in ALL.

    Conclusions:

    • The findings suggest a distinct developmental pathway for normal B-cell precursors compared to leukemic B-cell precursors in ALL.
    • The CD19 receptor's differential signaling in normal versus malignant B-cell precursors points to its potential role in the leukemogenesis of B-cell precursor ALL.
    • Further research into CD19-mediated signaling pathways could offer novel therapeutic targets for ALL.