International Immunology, Vol 10, 1367-1375, Copyright © 1998 by Oxford University Press
E Maraskovsky, JJ Peschon, H McKenna, M Teepe and A Strasser
IL-7 receptor-deficient (IL-7R(-/-)) mice are lymphopenic as a result of
defective cell production at early steps in both B and T lymphopoiesis. In
the bone marrow, there is an incomplete block in B cell development at the
transition from the pro-B to the pre-B cell stage. As a consequence,
peripheral lymphoid organs of IL-7R(-/-) mice contain abnormally low
numbers of mature surface (s) Ig-expressing B cells and this is accompanied
by a relative increase in immature sIg- B cells. Transgenic expression of
the anti-apoptotic protein Bcl-2 in IL- 7R(-/-) mice rescues the defect in
T cell development and in mature T cell function. The present report shows
that constitutive expression of Bcl-2 is incapable of rescuing B
lymphopoiesis in IL-7R(-/-) mice but can enhance survival of those mature B
cells which escape the developmental arrest. Thus the essential role of
IL-7R signaling in B lymphoid cells cannot be replaced by Bcl-2, indicating
that in B lymphopoiesis IL-7R signaling is necessary for promoting cell
division and/or for inhibiting a Bcl-2-insensitive pathway to apoptosis.
ARTICLES
Overexpression of Bcl-2 does not rescue impaired B lymphopoiesis in IL- 7 receptor-deficient mice but can enhance survival of mature B cells
Department of Immunobiology, Immunex Corp., Seattle, WA 98101, USA.
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