Reconstitution of CD8 T cells is essential for the prevention of multiple-organ cytomegalovirus histopathology after bone marrow transplantation

被引:101
作者
Podlech, J [1 ]
Holtappels, R [1 ]
Wirtz, N [1 ]
Steffens, HP [1 ]
Reddehase, MJ [1 ]
机构
[1] Univ Mainz, Inst Virol, D-55101 Mainz, Germany
关键词
D O I
10.1099/0022-1317-79-9-2099
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Cytomegalovirus (CMV) infection in the period of temporary immunodeficiency after haematoablative treatment and bone marrow transplantation (BMT) is associated with a risk of graft failure and multiple-organ CMV disease. The efficacy of immune system reconstitution is decisive for the prevention of CMV pathogenesis after BMT. Previous data in murine model systems have documented a redundancy in the immune effector mechanisms controlling CMV. CD8 T cells proved to be relevant but not irreplaceable as antiviral effecters. Specifically, in a state of long-term in vivo depletion of the CD8 T-cell subset, CD4 T cells were educed to become deputy effecters controlling CMV by a mechanism involving antiviral cytokines. It is of medical importance to know whether one can trust in this 'flexible defence' in all clinical settings. It ii demonstrated here that reconstitution of CD8 T cells is crucial for the prevention of fatal multiple-organ CMV disease under the specific conditions of BMT.
引用
收藏
页码:2099 / 2104
页数:6
相关论文
共 29 条
[1]   LUNGS ARE A MAJOR ORGAN SITE OF CYTOMEGALOVIRUS LATENCY AND RECURRENCE [J].
BALTHESEN, M ;
MESSERLE, M ;
REDDEHASE, MJ .
JOURNAL OF VIROLOGY, 1993, 67 (09) :5360-5366
[2]   THERAPY WITH MONOCLONAL-ANTIBODIES BY ELIMINATION OF T-CELL SUBSETS INVIVO [J].
COBBOLD, SP ;
JAYASURIYA, A ;
NASH, A ;
PROSPERO, TD ;
WALDMANN, H .
NATURE, 1984, 312 (5994) :548-551
[3]   Evidence against a key role for transforming growth factor-β1 in cytomegalovirus-induced bone marrow aplasia [J].
Dobonici, M ;
Podlech, J ;
Steffens, HP ;
Maiberger, S ;
Reddehase, MJ .
JOURNAL OF GENERAL VIROLOGY, 1998, 79 :867-876
[4]   MOLECULAR-CLONING AND PHYSICAL MAPPING OF MURINE CYTOMEGALOVIRUS DNA [J].
EBELING, A ;
KEIL, GM ;
KNUST, E ;
KOSZINOWSKI, UH .
JOURNAL OF VIROLOGY, 1983, 47 (03) :421-433
[5]  
Einsele H, 1998, MG VIROLOGY, V21, P106
[6]  
HOLT PG, 1985, IMMUNOLOGY, V54, P139
[7]   ANTIBODIES ARE NOT ESSENTIAL FOR THE RESOLUTION OF PRIMARY CYTOMEGALOVIRUS-INFECTION BUT LIMIT DISSEMINATION OF RECURRENT VIRUS [J].
JONJIC, S ;
PAVIC, I ;
POLIC, B ;
CRNKOVIC, I ;
LUCIN, P ;
KOSZINOWSKI, UH .
JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 179 (05) :1713-1717
[8]  
JONJIC S, 1990, J VIROL, V64, P5457
[9]   SITE-RESTRICTED PERSISTENT CYTOMEGALO-VIRUS INFECTION AFTER SELECTIVE LONG-TERM DEPLETION OF CD4+ LYMPHOCYTES-T [J].
JONJIC, S ;
MUTTER, W ;
WEILAND, F ;
REDDEHASE, MJ ;
KOSZINOWSKI, UH .
JOURNAL OF EXPERIMENTAL MEDICINE, 1989, 169 (04) :1199-1212
[10]   A neuroattenuated ICP34.5-deficient herpes simplex virus type 1 replicates in ependymal cells of the murine central nervous system [J].
Kesari, S ;
Lasner, TM ;
Balsara, KR ;
Randazzo, BP ;
Lee, VMY ;
Trojanowski, JQ ;
Fraser, NW .
JOURNAL OF GENERAL VIROLOGY, 1998, 79 :525-536