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Blood, Vol. 96 No. 1 (July 1), 2000:
pp. 9-23
REVIEW ARTICLE
Fates of human B-cell precursors
Tucker W. LeBien
From the Department of Laboratory Medicine and Pathology, University
of Minnesota Cancer Center, and Center for Immunology, University of
Minnesota, Minneapolis.
Development of mammalian B-lineage cells is characterized by
progression through a series of checkpoints defined primarily by
rearrangement and expression of immunoglobulin genes. Progression through these checkpoints is also influenced by stromal cells in the
microenvironment of the primary tissues wherein B-cell development
occurs, ie, fetal liver and bone marrow and adult bone marrow. This
review focuses on the developmental biology of human bone marrow
B-lineage cells, including perturbations that contribute to
the origin and evolution of B-lineage acute lymphoblastic leukemia and
primary immunodeficiency diseases characterized by agammaglobulinemia.
Recently described in vitro and in vivo models that support development
and expansion of human B-lineage cells through multiple checkpoints
provide new tools for identifying the bone marrow stromal cell-derived
molecules necessary for survival and proliferation. Mutations in genes
encoding subunits of the pre-B cell receptor and molecules involved in
pre-B cell receptor signaling culminate in X-linked and non-X-linked
agammaglobulinemia. A cardinal feature of these immunodeficiencies is
an apparent apoptotic sensitivity of B-lineage cells at the pro-B to
pre-B transition. On the other end of the spectrum is the apoptotic resistance that accompanies the development of B-lineage acute lymphoblastic leukemia, potentially a reflection of genetic
abnormalities that subvert normal apoptotic programs. The triad of
laboratory models that mimic the bone marrow microenvironment,
immunodeficiency diseases with specific defects in B-cell development,
and B-lineage acute lymphoblastic leukemia can now be integrated to
deepen our understanding of human B-cell development.
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