In the absence of T cells, natural killer cells protect from mortality due to HSV-1 encephalitis

被引:45
作者
Adler, H
Beland, JL
Del-Pan, NC
Kobzik, L
Sobel, RA
Rimm, IJ
机构
[1] Harvard Univ, Sch Med,Childrens Hosp, Dept Pediat Hematol Oncol, Dana Farber Canc Inst,Dept Pediat, Boston, MA 02115 USA
[2] Brigham & Womens Hosp, Physiol Program, Harvard Sch Publ Hlth, Boston, MA 02115 USA
[3] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA
[4] Stanford Univ, Sch Med, Lab Serv, Palo Alto Vet Affairs Hlth Care Syst, Stanford, CA 94305 USA
[5] Stanford Univ, Sch Med, Dept Pathol, Stanford, CA 94305 USA
基金
美国国家卫生研究院;
关键词
HSV-1; NK cells; encephalitis;
D O I
10.1016/S0165-5728(98)00236-7
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The importance of natural killer (NK) cells in the resistance to herpes simplex virus type 1 (HSV-I), a common infection of immunocompromised patients, is unclear. Previous data on the role of NK cells in murine HSV-I infection has been contradictory. Adoptive transfer studies suggested that NK cells mediated resistance to HSV-1, but in vivo depletion approaches demonstrated that NK cells were not important. We studied the course of HSV-I infection after intranasal (i.n.) inoculation of E26 mice (lacking NK and T cells), T cell knockout (T cell ko) mice (lacking T cells only), or normal control mice. The E26 mice showed greater mortality and an impaired ability to clear virus from lung and brain compared to T cell ko mice and control mice, and had severe necrotizing HSV-1 encephalitis. Therefore, the data support the hypothesis that NK cells play an important role in the natural defense of murine HSV-1 infection. (C) 1999 Elsevier Science B.V. AU rights reserved.
引用
收藏
页码:208 / 213
页数:6
相关论文
共 38 条
[1]   Suppression of Herpes simplex virus type 1 (HSV-1)-induced pneumonia in mice by inhibition of inducible nitric oxide synthase (iNOS, NOS2) [J].
Adler, H ;
Beland, JL ;
DelPan, NC ;
Kobzik, L ;
Brewer, JP ;
Martin, TR ;
Rimm, IJ .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 185 (09) :1533-1540
[2]   SEVERE HERPESVIRUS INFECTIONS IN AN ADOLESCENT WITHOUT NATURAL-KILLER CELLS [J].
BIRON, CA ;
BYRON, KS ;
SULLIVAN, JL .
NEW ENGLAND JOURNAL OF MEDICINE, 1989, 320 (26) :1731-1735
[3]   Activation and function of natural killer cell responses during viral infections [J].
Biron, CA .
CURRENT OPINION IN IMMUNOLOGY, 1997, 9 (01) :24-34
[4]   PATHOGENESIS OF MURINE CYTOMEGALOVIRUS-INFECTION IN NATURAL-KILLER CELL-DEPLETED MICE [J].
BUKOWSKI, JF ;
WODA, BA ;
WELSH, RM .
JOURNAL OF VIROLOGY, 1984, 52 (01) :119-128
[5]  
BUKOWSKI JF, 1986, J IMMUNOL, V136, P3481
[6]  
BUKOWSKI JF, 1983, J IMMUNOL, V131, P1531
[7]   An experimental model of idiopathic pneumonia syndrome after bone marrow transplantation .1. The roles of minor H antigens and endotoxin [J].
Cooke, KR ;
Kobzik, L ;
Martin, TR ;
Brewer, J ;
Delmonte, J ;
Crawford, JM ;
Ferrara, JLM .
BLOOD, 1996, 88 (08) :3230-3239
[8]  
GODENY EK, 1987, J IMMUNOL, V139, P913
[9]   Infected cell protein (ICP)47 enhances herpes simplex virus neurovirulence by blocking the CD8+ T cell response [J].
Goldsmith, K ;
Chen, W ;
Johnson, DC ;
Hendricks, RL .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 187 (03) :341-348
[10]  
Griffin D E, 1992, Semin Immunol, V4, P111