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Blood, 1 May 2002, Vol. 99, No. 9, pp. 3350-3359
IMMUNOBIOLOGY
Perturbation of B-cell development in mice overexpressing the
Bcl-2 homolog A1
Peter I. Chuang,
Samantha Morefield,
Chien-Ying Liu,
Stephen Chen,
John M. Harlan, and
Dennis M. Willerford
From the Departments of Medicine and Immunology,
University of Washington, Seattle.
Decisions about cell survival or death are central components of
adaptive immunity and occur at several levels in immune system development and function. The Bcl-2 family of homologous proteins plays
an important role in these decisions in lymphoid cells. Bcl-2, Bcl-xL,
and A1 are differentially expressed during B- and T-cell development,
and they have shared and distinct roles in regulating cell death. We
sought to gain insight into the role of A1 in immune system development
and function. A murine A1-a transgene was expressed under
the control of the Eµ enhancer, and mice with A1 overexpression in B-
and T-cell lineages were derived. Thymocytes and early B cells in
Eµ-A1 mice showed extended survival. B-lineage development was
altered, with expansion of the pro-B cell subset at the expense of
pre-B cells, suggesting an impairment of the pro- to pre-B-cell
transition. This early B-cell phenotype resembled Eµ-Bcl-xL mice but
did not preferentially rescue cells with completed V(D)J rearrangements
of the immunoglobulin heavy chain. In contrast to Eµ-Bcl-2
transgenes, A1 expression in pro-B cells did not rescue pre-B-cell
development in SCID mice. These studies indicate that A1 protects
lymphocytes from apoptosis in vitro but that it has lineage- and
stage-specific effects on lymphoid development. Comparison with the
effects of Bcl-2 and Bcl-xL expressed under similar control elements
supports the model that antiapoptotic Bcl-2 homologs interact
differentially with intracellular pathways affecting development and
apoptosis in lymphoid cells.
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