Endogenous TGF-beta contributes to the induction of the EBV lytic cycle in two Burkitt lymphoma cell lines.
A low proportion of cells in the BL lines P3HR-I and Akata enter spontaneously into the EBV lytic cycle, detectable by the expression of early antigens (EA). We found that both lines produce the active and inactive forms of TGF beta. It was shown earlier that a larger number of cells can be induced to enter the lytic cycle by exposing P3HR-I to phorbol esters and n-butyrate and the surface IgG-positive Akata cells to anti-IgG. We now show that the same treatments raise the level of active TGF beta release. Exposure to anti-TGF beta antibodies reduced EA induction by 75-85%. Our results indicate that induction of the viral productive cycle by the above-mentioned reagents is at least partly dependent on the activation of endogenous TGF beta production.
di Renzo
L
L
Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.
Altiok
A
A
Klein
G
G
Klein
E
E
D002051:Burkitt Lymphoma / Q000382:microbiology*; D002087:Butyrates / Q000494:pharmacology; D002455:Cell Division / Q000187:drug effects; D004854:Herpesvirus 4, Human / Q000254:growth & development*; D006801:Humans; D015240:Phorbol 12,13-Dibutyrate / Q000494:pharmacology; D016212:Transforming Growth Factor beta / Q000494:pharmacology / Q000502:physiology*; D014407:Tumor Cells, Cultured; D017735:Virus Latency; D014779:Virus Replication
D002087:Butyrates; D016212:Transforming Growth Factor beta; D015240:Phorbol 12,13-Dibutyrate