A mechanism of T cell regulation of Epstein-Barr virus latency.
The tumorigenic potential of B lymphocytes latently infected with EBV is effectively controlled by T cell immunity. The mechanisms of this T cell regulation, however, are incompletely understood. In this study, T lymphocytes were found to proliferate in response to serum-free supernatants of EBV-immortalized cells and to deplete them of growth factors required by the immortalized B cells for autocrine growth. Lactic acid was reported to account for approximately 90% of the autocrine growth factor activity in serum-free supernatants of EBV-immortalized cell lines. Synthetic lactic acid was now found to promote growth in activated T cells. In addition, B cell suppression resulting from coculture of EBV-infected B cells with autologous T cells was reversed by the addition of supernatants from EBV-immortalized cell lines. Thus, T cell competition for growth factors produced and utilized by EBV-immortalized B cells for continuous proliferation may represent an important and novel regulatory mechanism for the maintenance of EBV latency in B lymphocytes.
Frugoni
P
P
Center for Biologics Evaluation and Research, FDA, Bethesda, Maryland 20892.
Pike
S E
SE
Tosato
G
G
D001402:B-Lymphocytes / Q000166:cytology / Q000382:microbiology*; D015496:CD4-Positive T-Lymphocytes / Q000502:physiology; D016827:CD8 Antigens / Q000032:analysis; D002478:Cells, Cultured; D003470:Culture Media; D006133:Growth Substances / Q000502:physiology*; D004854:Herpesvirus 4, Human / Q000254:growth & development*; D006801:Humans; D066298:In Vitro Techniques; D007773:Lactates / Q000494:pharmacology; D008213:Lymphocyte Activation; D013601:T-Lymphocytes / Q000502:physiology*; D014412:Tumor Virus Infections / Q000382:microbiology*
D016827:CD8 Antigens; D003470:Culture Media; D006133:Growth Substances; D007773:Lactates