Interleukin-10 prevents spontaneous death of germinal center B cells by induction of the bcl-2 protein.
AUTOR(ES)
Levy, Y
RESUMO
In this study, we show that IL-10 enhances in vitro the viability of purified splenic B cells. There was a two- to threefold increase in recovery of viable cells during a 15-d culture period in the presence of IL-10. This effect was abolished by neutralizing antibodies to IL-10. The survival of large splenic B cells, which mostly represent follicular center cells, was similarly increased. The in vitro rescue from spontaneous death of the latter cells is known to involve a bcl-2-dependent pathway. We therefore investigated whether IL-10 might affect bcl-2 expression. Unseparated B cells as well as large splenic B cells displayed a strong expression of bcl-2 protein by immunofluorescence at days 2-7 of culture in the presence of IL-10. Other lymphokines such as IL-2 and IL-4 were able to trigger only a transient and faint expression of bcl-2; moreover, this effect was abolished by anti-IL-10 mAb. Inasmuch as activated B cells can produce their own IL-10, this lymphokine may play a crucial role in relieving from apoptosis those B cells that encounter their antigen in B cell follicles.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=293803Documentos Relacionados
- bcl-2 inhibits death of central neural cells induced by multiple agents.
- Developmental regulation of the Bcl-2 protein and susceptibility to cell death in B lymphocytes.
- Estrogen up-regulates Bcl-2 and blocks tolerance induction of naïve B cells
- Bcl-2 prevents apoptotic mitochondrial dysfunction by regulating proton flux
- Interleukin-10 inhibits apoptotic cell death in infectious mononucleosis T cells.