Control of interferon, migration inhibition factor, and expression of virus capsid antigens in Burkitt's lymphoma-derived cell lines: role of L-arginine.

Abstract

The effects of an arginine-utilizing mycoplasma, Mycoplasma arginini, and of varying levels of arginine in the growth media of the Epstein-Barr virus (EBV)-containing EB1 and EB3 cell lines, and the EBV-free RPMI 1788 cell line, were studied. l-Arginine, at a concentration of 0.1 mM in the growth medium, led to a reduction of the EBV capsid antigen content of the EB1 and EB3 cells lines as determined by indirect immunofluorescence, and M. arginini infection enhanced this reduction. The synthesis of two immune products, interferon and macrophage migration inhibition factor, was enhanced by growing the cell lines in medium containing arginine at a concentration of 0.1 mM, but the RPMI 1788 cell line produced much less of both products than EB1 or EB3 under these conditions. Infection of the cell lines with M. arginini reduced the amount of interferon produced and completely inhibited macrophage migration inhibition factor synthesis. The addition of arginine to a final concentration of 0.6 mM in the growth medium caused a dual effect: the EB1 and EB3 cell lines maintained the original level of EBV capsid antigens, even when infected with M. arginini; immune product synthesis was greatly reduced or completely inhibited by the addition of arginine, and M. arginini infection caused no further reduction of immune product synthesis.