Overexpression of Bcl-2 does not rescue impaired B lymphopoiesis in IL-7 receptor-deficient mice but can enhance survival of mature B cells
- Author(s)
- Maraskovsky, E; Peschon, JJ; McKenna, H; Teepe, M; Strasser, A;
- Details
- Publication Year 1998-09,Volume 10,Issue #9,Page 1367-1375
- Journal Title
- INTERNATIONAL IMMUNOLOGY
- Publication Type
- Journal Article
- Abstract
- 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 slg(-) 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 Eel-a-insensitive pathway to apoptosis.
- Publisher
- OXFORD UNIV PRESS
- Keywords
- DEFECTIVE LYMPHOID DEVELOPMENT; INTERLEUKIN-7 RECEPTOR; GAMMA-CHAIN; CYCLE PROGRESSION; T-LYMPHOPOIESIS; TRANSGENIC MICE; EXPRESSION; MURINE; DEATH; LYMPHOCYTES
- Publisher's Version
- https://doi.org/10.1093/intimm/10.9.1367
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1998-09-01 12:00:00