Interferon amplifies complement activation by Burkitt's lymphoma cells

E. Yefenof*, I. McConnell

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

Interferon was originally described as an antiviral agent produced shortly after onset of infection with most viruses1. However, in addition to inducing an antiviral state, interferon inhibits cell division2, increases the expression of cell-surface antigens3, boosts the cytotoxic activity of natural killer (NK) cells4,5 and modulates several immune functions of lymphocytes and macrophages6-9. Moreover, a special class of interferon (immune interferon or IFN-γ) is produced by T cells following stimulation with antigen or interaction with mitogens 10,11. The different methods by which interferon is induced and its multiple effects suggest that it may be part of a first-line defence system controlling the spread of virus infections and the proliferation of modified 'self' cells that have been affected by virus infection or neoplastic transformation12. The ability of certain human lymphoma cells to activate the alternative pathway of complement is well established 13-15. Here we show that monoclonal antibody-purified interferon can amplify the ability of certain tumour cells to activate complement via the alternative pathway. This demonstration may reflect an additional, as yet unknown, role of interferon in inducing nonspecific anti-tumour immunity.

Original languageEnglish
Pages (from-to)684-685
Number of pages2
JournalNature
Volume313
Issue number6004
DOIs
StatePublished - 1985

Fingerprint

Dive into the research topics of 'Interferon amplifies complement activation by Burkitt's lymphoma cells'. Together they form a unique fingerprint.

Cite this