Induction of apoptosis by dexamethasone in the B cell lineage.
Immunopharmacology
; 40(1): 67-76, 1998 Jul.
Article
en En
| MEDLINE
| ID: mdl-9776480
The susceptibility to induction of apoptosis by the synthetic glucocorticoid, dexamethasone (Dex), was analysed at different stages of B cell maturation. Cells of the 70Z/3 pre-B cell line, expressing cytoplasmic mu chains, and LPS-stimulated 70Z/3 cells, expressing surface IgM, were used as a model of differentiation of pre-B cells into immature B cells. Cell proliferation and cell cycle progression were similarly inhibited by Dex (100 nM) in both naive 70Z/3 pre-B cells and in LPS-stimulated 70Z/3 cells. In contrast, Dex failed to affect apoptosis of naive 70Z/3 cells while it increased that of LPS-stimulated 70Z/3 cells. Splenic mature B lymphocytes were highly susceptible to Dex-induced apoptosis since subphysiological doses (5 nM) increased the frequency of apoptotic cells to more than 80%. On the other hand, the treatment of B lymphocytes with LPS, which led to proliferation and differentiation into immunoblasts, decreased the susceptibility to Dex-induced apoptosis. These effects were mediated by the glucocorticoid receptor since they were abrogated by the RU 486 antagonist. The response of B cells to glucocorticoids is thus dependent on their stage of differentiation.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Dexametasona
/
Linfocitos B
/
Apoptosis
/
Glucocorticoides
Límite:
Animals
Idioma:
En
Revista:
Immunopharmacology
Año:
1998
Tipo del documento:
Article
País de afiliación:
Francia
Pais de publicación:
Países Bajos