Tumor dormancy and cell signaling: anti-mu-induced apoptosis in human B-lymphoma cells is not caused by an APO-1-APO-1 ligand interaction.
AUTOR(ES)
Racila, E
RESUMO
Signal transduction initiated by crosslinking of antigen-specific receptors on T- and B-lymphoma cells induces apoptosis. In T-lymphoma cells, such crosslinking results in upregulation of the APO-1 ligand, which then interacts with induced or constitutively expressed APO-1, thereby triggering apoptosis. Here we show that crosslinking the membrane immunoglobulin on human lymphoma cells (Daudi) (that constitutively express APO-1) does not induce synthesis of APO-1 ligand. Further, a noncytotoxic fragment of anti-APO-1 antibody that blocks T-cell-receptor-mediated apoptosis in T-lymphoma cells does not block anti-mu-induced apoptosis. Hence, in B-lymphoma cells, apoptosis induced by signaling via membrane IgM is not mediated by the APO-1 ligand.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=39928Documentos Relacionados
- Simultaneous expression of mu- and gamma-chain mRNA in cloned murine B-lymphoma cell lines.
- Fast and high-affinity binding of B-lymphotropic papovavirus to human B-lymphoma cell lines.
- Cancer dormancy and cell signaling: Induction of p21waf1 initiated by membrane IgM engagement increases survival of B lymphoma cells
- B-lymphoma cells process and present their endogenous immunoglobulin to major histocompatibility complex-restricted T cells.
- Epstein-Barr virus (EBV) induces expression of B-cell activation markers on in vitro infection of EBV-negative B-lymphoma cells.