ANTIVIRAL ACTION OF TUMOR NECROSIS FACTOR IN HUMAN-FIBROBLASTS IS NOT MEDIATED BY B-CELL STIMULATORY FACTOR-II IFN-BETA-2, AND IS INHIBITED BY SPECIFIC ANTIBODIES TO IFN-BETA

  • 1 March 1988
    • journal article
    • research article
    • Vol. 140  (5) , 1566-1570
Abstract
A protein termed IFN-.beta.2, originally described on the basis of antiviral activity and antigenic cross-reactivity with the classical IFN-.beta., is now known to be identical with the independently isolated B cell stimulatory factor (BSF-2). Earlier it was suggested that IFN-.beta.2 (i.e., BSF-2) mediates the antiviral action of TNF in human fibroblasts. We examined Escherichia coli-derived recombinant preparations of human IFN-.beta. and BSF-2 for antiviral activity and plasmacytoma growth factor (PCT-GF) activity. IFN-.beta. had antiviral activity but showed no PCT-GF activity. BSF-2 showed potent PCT-GF activity but lacked antiviral activity. Antiviral activity of IFN-.beta. was neutralized by polyclonal antibodies and mAb to IFN-.beta., but not by antibody to rBSF-2. PCT-GF activity of BSA-2 was neutralized by antibody to rBSF-2, but not by antibodies neutralizing the antiviral action of IFN-.beta.. Five mAb and a polyclonal antibody to human IFN-.beta. failed to react with BSF-2 in a solid phase RIA and antibody to BSF-2 did not react with IFN-.beta., PCT-GF activity in supernatants of human FS-4 fibroblasts stimulated with TNF, IL-1 or poly(I).cntdot.poly(C) was neutralized by antibody to rBSF-2, but not by antibodies neutralizing the antiviral activity of IFN-.beta.. Finally, the antiviral activity of TNF in FS-4 cultures was neutralized by antibodies to IFN-.beta. but not by antibodies to BSA-2. Taken together, these results support the view that the antiviral action of TNF in human fibroblasts is mediated by IFN-.beta., and not by BSF-2/IFN-.beta.2 that apparently lacks significant antiviral activity.