| First Author | Foote LC | Year | 1996 |
| Journal | J Immunol | Volume | 157 |
| Issue | 5 | Pages | 1878-85 |
| PubMed ID | 8757305 | Mgi Jnum | J:34897 |
| Mgi Id | MGI:82352 | Doi | 10.4049/jimmunol.157.5.1878 |
| Citation | Foote LC, et al. (1996) Intracellular signaling for inducible antigen receptor-mediated Fas resistance in B cells. J Immunol 157(5):1878-85 |
| abstractText | CD40 ligand-activated B cells are sensitive targets for CD4+ Th1 effector cells that kill in a Fas-dependent fashion. Susceptibility to apoptosis is counteracted by Ag receptor binding that produces a state of resistance to Fas engagement in otherwise sensitive targets. In the present study, protection from Th1-mediated apoptosis was found to be induced by protein kinase C and calcium signals, which in combination mimicked the level of Fas resistance produced by surface Ig engagement. Signaling for Fas resistance did not alter Fas expression. Furthermore, B cells that were protected against Th1-mediated apoptosis were also resistant to apoptosis mediated by soluble, rFas ligand. Taken together, these results indicate that signaling for protection against Fas-mediated apoptosis does not depend on alteration of the interaction between B cell target and Th1 effector populations. Instead, surface IgM-derived protein kinase C and calcium signals appear to produce an intracellular change in the Fas signaling pathway that develops over a period of hours and interferes with the apoptotic process through a mechanism that depends on protein synthesis. |
