Type I interferon induces inhibitory 16-kD CCAAT/ enhancer binding protein (C/EBP)beta, repressing the HIV-1 long terminal repeat in macrophages: pulmonary tuberculosis alters C/EBP expression, enhancing HIV-1 replication.
Type I interferon induces inhibitory 16-kD CCAAT/ enhancer binding protein (C/EBP)beta, repressing the HIV-1 long terminal repeat in macrophages: pulmonary tuberculosis alters C/EBP expression, enhancing HIV-1 replication.
复制标题
DOI：
10.1084/jem.188.7.1255
复制
发表时间：
1998-10-05
期刊：
影响因子：
--
通讯作者：
Weiden M
中科院分区：
文献类型：
--
作者：
Honda Y;Rogers L;Nakata K;Zhao BY;Pine R;Nakai Y;Kurosu K;Rom WN;Weiden M
We have previously observed that HIV-1 replication is suppressed in uninflamed lung and increased during tuberculosis. In vitro THP-1 cell–derived macrophages inhibited HIV-1 replication after infection with Mycobacterium tuberculosis. Suppression of HIV-1 replication was associated with inhibition of the HIV-1 long terminal repeat (LTR) and induction of ISGF-3, a type I interferon (IFN)–specific transcription factor. Repression of the HIV-1 LTR required intact CCAAT/enhancer binding protein (C/EBP) sites. THP-1 cell–derived macrophages infected with M. tuberculosis, lipopolysaccharide, or IFN-β induced the 16-kD inhibitory C/EBPβ isoform and coincidentally repressed HIV-1 LTR transcription. C/EBPβ was the predominant C/EBP family member produced in THP-1 macrophages during HIV-1 LTR repression. In vivo, alveolar macrophages from uninflamed lung strongly expressed inhibitory 16-kD C/EBPβ, but pulmonary tuberculosis abolished inhibitory C/EBPβ expression and induced a novel C/EBP DNA binding protein. Therefore, in vitro, proinflammatory stimulation produces an IFN response inhibiting viral replication by induction of a C/EBPβ transcriptional repressor. THP-1 cell–derived macrophages stimulated with type I IFN are similar to alveolar macrophages in the uninflamed lung in vivo. In contrast, the cellular immune response in active pulmonary tuberculosis disrupts this innate immunity, switching C/EBP expression and allowing high level viral replication.
登录
查看更多内容
影响因子：
56.9
作者：
MULLER, U;STEINHOFF, U;AGUET, M
通讯作者：
AGUET, M
DOI：
10.1073/pnas.92.24.11284
发表时间：
1995-11-21
影响因子：
11.1
作者：
HWANG, SY;HERTZOG, PJ;KOLA, I
通讯作者：
KOLA, I
影响因子：
15.9
作者：
BERNSTEIN, MS;TONGSTARKSEN, SE;LOCKSLEY, RM
通讯作者：
LOCKSLEY, RM
DOI：
10.1073/pnas.90.17.8219
发表时间：
1993-09-01
影响因子：
11.1
作者：
OSSIPOW, V;DESCOMBES, P;SCHIBLER, U
通讯作者：
SCHIBLER, U
DOI：
10.1164/ajrccm.155.3.9117038
发表时间：
1997-03-01
影响因子：
24.7
作者：
Nakata, K;Rom, WN;Weiden, M
通讯作者：
Weiden, M