Contribution of T cells to mortality in neurovirulent Sindbis virus encephalomyelitis

被引：53

作者：

Rowell, JF ^{[1
]}

Griffin, DE ^{[1
]}

机构：

[1] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, W Harry Feinstone Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2002年 / 127卷 / 1-2期

基金：

美国国家卫生研究院;

关键词：

T lymphocytes; infectious immunity-virus; transgenic/knockout;

D O I：

10.1016/S0165-5728(02)00108-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：

Intranasal inoculation of C57BL/6 mice with a neurovirulent strain of Sindbis virus (SV) results in fatal encephalomyelitis. Mice with selective immune deficiencies were studied to determine the role of the immune response in fatal outcome. Mortality was decreased in mice deficient in alphabeta, but not gammadelta, T cells demonstrating a contribution of alphabeta cells. Mice lacking either CD4(+) or CD8(+) T cells also had reduced mortality and mice lacking interferon (IFN)-gamma were completely protected. Clearance of infectious virus was identical in mice without T cells or IFN-gamma, but clearance of viral RNA was delayed compared to normal mice. Mice unable to produce antibody, perform, Fas, TNF-alpha. receptor1, IL-6 or IL-12 were not protected. These data suggest that T cells contribute to fatal acute viral encephalomyelitis through the production of IFN-gamma. (C) 2002 Elsevier Science B.V. All rights reserved.

引用

页码：106 / 114

页数：9

共 65 条

[1] Functional maturation of adult mouse resting microglia into an APC is promoted by granulocyte-macrophage colony-stimulating factor and interaction with Th1 cells [J].