CD40 ligand incorporated into the HIV envelope and expression of activation-induced cytidine deaminase may help explain the relationship between HIV load and Burkitt lymphoma.
Thus, the growth inhibition and apoptosis-inducing activity of srhCD40L via CD40-CD40 ligand interaction on Burkitt lymphoma cells was confirmed, and these effects may be attributable to the suppression of NF-kappaB binding activity.
We have used Ramos germinal center (GC)-derived Burkitt's lymphoma (BL) cells as a model system to compare some of the early signaling events of TNF-alpha and CD40L on the NF-kappaB and c-Jun amino-terminal kinase (JNK) pathways.
Culture of group I BL lines with CD40L resulted in significant growth arrest (without apoptosis) that, for L3055 cells, was sustained for 7 to 9 days after 72 hours of exposure.
Coculture of Ramos Burkitt's lymphoma line cells with irradiated SAg-reactive CD4+ T cells with SAg or CD40L+ Jurkat T cells results in B cell apoptosis, evidenced by reduced cell viability and DNA laddering.