Investigation of IFN type-I receptor and IFN regulatory factor expression relating to induction of 2',5'-oligoadenylate synthetase in cells persistently infected with the mumps virus

被引:12
作者
Fujii, N
Yokosawa, N
Ishida, S
Shirakawa, S
Kubota, T
Indoh, T
Fujinaga, K
Yashiki, T
机构
[1] SAPPORO MED UNIV,SCH MED,CANC RES INST,SAPPORO,HOKKAIDO 060,JAPAN
[2] HOKKAIDO UNIV,COLL MED TECHNOL,LAB TECHNOL,SAPPORO,HOKKAIDO 060,JAPAN
关键词
2'; 5'-oligoadenylate synthetase (2-5AS); interferon; interferon receptor; RT-PCR; IRF-1; IRF-2; mumps virus; persistent infection;
D O I
10.1111/j.1348-0421.1996.tb01141.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Poor induction of interferon-induced 2', 5'-oligoadenylate synthetase (2-5AS) activity has been demonstrated in cells persistently infected with the mumps virus or human T-lymphotropic virus type-I (HTLV-I). The suppression of 2-5AS induction is the result of the repression of 2-5AS gene expression at the transcription level. In a general way, after the binding of interferon-alpha (IFN-alpha) to cell surface-specific receptors, expression of 2-5AS gene is thought to be regulated by some transacting factors, IFN-regulatory factors (IRF-1 and IRF-2) and the IFN-stimulated gene factor (ISGF-3, a complex consisting of STAT-1 alpha, STAT-2 and p48). To clarify the cause of the suppression mechanism(s), fluctuation in the number of IFN receptors and the levels of mRNAs in both IRF-1 and IRF-2 were examined in cells persistently infected with the mumps virus (FLMT and KBMT). There were few defferences in the number of IFN receptors and the level of IRF-2 mRNA between persistently infected cells and uninfected control cells. After the treatment of cells with IFN, a slight reduction of IRF-1 mRNA was found in persistently infected cells as compared with that of the uninfected control cells.
引用
收藏
页码:777 / 781
页数:5
相关论文
共 20 条
[11]   ABSENCE OF THE TYPE-I IFN SYSTEM IN EC CELLS - TRANSCRIPTIONAL ACTIVATOR (IRF-1) AND REPRESSOR (IRF-2) GENES ARE DEVELOPMENTALLY REGULATED [J].
HARADA, H ;
WILLISON, K ;
SAKAKIBARA, J ;
MIYAMOTO, M ;
FUJITA, T ;
TANIGUCHI, T .
CELL, 1990, 63 (02) :303-312
[12]   STRUCTURALLY SIMILAR BUT FUNCTIONALLY DISTINCT FACTORS, IRF-1 AND IRF-2, BIND TO THE SAME REGULATORY ELEMENTS OF IFN AND IFN-INDUCIBLE GENES [J].
HARADA, H ;
FUJITA, T ;
MIYAMOTO, M ;
KIMURA, Y ;
MARUYAMA, M ;
FURIA, A ;
MIYATA, T ;
TANIGUCHI, T .
CELL, 1989, 58 (04) :729-739
[13]   SEQUENCE OF A CDNA CODING FOR HUMAN IRF-2 [J].
ITOH, S ;
HARADA, H ;
FUJITA, T ;
MIMURA, T ;
TANIGUCHI, T .
NUCLEIC ACIDS RESEARCH, 1989, 17 (20) :8372-8372
[14]   INHIBITION OF INTERFERON-INDUCIBLE GENE-EXPRESSION BY ADENOVIRUS E1A PROTEINS - BLOCK IN TRANSCRIPTIONAL COMPLEX-FORMATION [J].
KALVAKOLANU, DVR ;
BANDYOPADHYAY, SK ;
HARTER, ML ;
SEN, GC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (17) :7459-7463
[15]   SEQUENCE OF A CDNA CODING FOR HUMAN IRF-1 [J].
MARUYAMA, M ;
FUJITA, T ;
TANIGUCHI, T .
NUCLEIC ACIDS RESEARCH, 1989, 17 (08) :3292-3292
[16]   CRITICAL ROLE OF A COMMON TRANSCRIPTION FACTOR, IRF-1, IN THE REGULATION OF IFN-BETA AND IFN-INDUCIBLE GENES [J].
REIS, LFL ;
HARADA, H ;
WOLCHOK, JD ;
TANIGUCHI, T ;
VILCEK, J .
EMBO JOURNAL, 1992, 11 (01) :185-193
[17]   Interferon-Dependent Tyrosine Phosphorylation of a Latent Cytoplasmic Transcription Factor (Reprinted from AAAS, vol 257, pg 809-813, 1992) [J].
Schindler, Chris ;
Shuai, Ke ;
Prezioso, Vincent R. ;
Darnell, James E., Jr. .
JOURNAL OF IMMUNOLOGY, 2011, 187 (11) :5489-5493
[18]   INTERFERON ACTIVATION OF THE TRANSCRIPTION FACTOR STAT91 INVOLVES DIMERIZATION THROUGH SH2-PHOSPHOTYROSYL PEPTIDE INTERACTIONS [J].
SHUAI, K ;
HORVATH, CM ;
HUANG, LHT ;
QURESHI, SA ;
COWBURN, D ;
DARNELL, JE .
CELL, 1994, 76 (05) :821-828
[19]   A PROTEIN TYROSINE KINASE IN THE INTERFERON-ALPHA/BETA SIGNALING PATHWAY [J].
VELAZQUEZ, L ;
FELLOUS, M ;
STARK, GR ;
PELLEGRINI, S .
CELL, 1992, 70 (02) :313-322
[20]   CELL-SURFACE RECEPTOR-MEDIATED INTERNALIZATION OF INTERFERON - ITS RELATION TO THE ANTIVIRAL ACTIVITY OF INTERFERON [J].
YONEHARA, S ;
ISHII, A ;
YONEHARATAKAHASHI, M .
JOURNAL OF GENERAL VIROLOGY, 1983, 64 (NOV) :2409-2418