Subversion of B lymphocyte signaling by infectious agents

被引:15
作者
Hasler, P
Zouali, M
机构
[1] Felix Platter Hosp, Rheumatol Univ Klin, Basel, Switzerland
[2] Hop Broussais, INSERM, U430, F-75674 Paris, France
关键词
B lymphocyte; signaling; infectious agent; EBV;
D O I
10.1038/sj.gene.6363941
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Infectious agents and their hosts interact in a complex manner, involving not only superficially apparent mechanisms, but also the signaling machinery that governs host cells responses. Thus, signaling events, surface molecule expression, and transcriptional control may be affected in various cell types, with profound consequences for the function of individual cells and organ systems. Studies of the biochemistry of cell signaling and cell invasion by infectious agents have begun to detail the interplay between elements of infectious organisms and the host at the molecular level. Consequently, the resulting interferences with lymphocyte signaling may disturb the function of the immune system. In B cells, alterations of immune receptor signaling has implications for human diseases. By affecting the mechanisms of the host's immune defense, this may not only lead to inadequate elimination of an infectious agent, but also to autoimmunity or neoplasia.
引用
收藏
页码:95 / 103
页数:9
相关论文
共 104 条
[1]   Modulation of major histocompatibility class II protein expression by varicella-zoster virus [J].
Abendroth, A ;
Slobedman, B ;
Lee, E ;
Mellins, E ;
Wallace, M ;
Arvin, AM .
JOURNAL OF VIROLOGY, 2000, 74 (04) :1900-1907
[2]   NOTCH SIGNALING [J].
ARTAVANISTSAKONAS, S ;
MATSUNO, K ;
FORTINI, ME .
SCIENCE, 1995, 268 (5208) :225-232
[3]   BINDING-SITES OF THE EPSTEIN-BARR-VIRUS AND C3D RECEPTOR (CR-2, CD21) FOR ITS 3 INTRACELLULAR LIGANDS, THE P53 ANTIONCOPROTEIN, THE P68 CALCIUM-BINDING PROTEIN AND THE NUCLEAR P120 RIBONUCLEOPROTEIN [J].
BAREL, M ;
BALBO, M ;
GAUFFRE, A ;
FRADE, R .
MOLECULAR IMMUNOLOGY, 1995, 32 (06) :389-397
[4]   TUMORIGENICITY OF CELLS TRANSFORMED BY ADENOVIRUS-TYPE-12 BY EVASION OF T-CELL IMMUNITY [J].
BERNARDS, R ;
SCHRIER, PI ;
HOUWELING, A ;
BOS, JL ;
VANDEREB, AJ ;
ZIJLSTRA, M ;
MELIEF, CJM .
NATURE, 1983, 305 (5937) :776-779
[5]  
Bouillie S, 1999, J IMMUNOL, V162, P136
[6]  
BRADBURY LE, 1992, J IMMUNOL, V149, P2841
[7]  
Busch LK, 1999, J IMMUNOL, V162, P2555
[8]   Epstein-Barr virus LMP2A-induced B-cell survival in two unique classes of EμLMP2A transgenic mice [J].
Caldwell, RG ;
Brown, RG ;
Longnecker, R .
JOURNAL OF VIROLOGY, 2000, 74 (03) :1101-1113
[9]   Epstein-Barr virus LMP2A drives B cell development and survival in the absence of normal B cell receptor signals [J].
Caldwell, RG ;
Wilson, JB ;
Anderson, SJ ;
Longnecker, R .
IMMUNITY, 1998, 9 (03) :405-411
[10]  
CALLARD RE, 1992, J IMMUNOL, V148, P2983