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Cells resistant to interferon are defective in activation of a promoter‐binding factor.
Author(s) -
Kessler D. S.,
Pine R.,
Pfeffer L. M.,
Levy D. E.,
Darnell J. E.
Publication year - 1988
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1988.tb03262.x
Subject(s) - biology , interferon , interferon gamma , microbiology and biotechnology , genetics , cytokine
Human cultured cell lines deficient in their ability to respond to type I interferon (IFN) fail to interrupt cellular proliferation or to induce an antiviral state following exposure to IFN alpha. Comparison of non‐responsive Daudi and HeLa cell lines with IFN‐responsive partner cell lines and examination of non‐responsive Raji cells showed that the defective cell lines expressed type I IFN receptors of typical number and affinity and bound IFN equivalently compared to the normal cells. However, transcriptional induction of interferon‐stimulated genes (ISGs) was greatly reduced and delayed in these cell lines, leading to reduced accumulation of ISG mRNA. Furthermore, the rapid activation of IFN‐stimulated promoter binding factors whose appearance correlates with ISG transcriptional induction, did not occur in non‐responsive cells. Thus, the primary defect of these cells leading to an impaired physiological response to IFN appears to be an inability to activate promoter‐binding factors necessary to trigger ISG transcription, an obligate early step in antiviral and antiproliferative physiology.