TY - JOUR
T1 - Contribution of T cells to mortality in neurovirulent Sindbis virus encephalomyelitis
AU - Rowell, Jennifer F.
AU - Griffin, Diane E.
N1 - Funding Information:
We thank Dr. Michael Havert and Gwendolyn Binder for helpful discussion and technical advice. We thank Dr. Teresa Colella for critical reading of the manuscript. This work was supported by Research Grant NS18596 from the National Institutes of Health (DEG) and by a postdoctoral fellowship from the National Multiple Sclerosis Society (JFR).
PY - 2002
Y1 - 2002
N2 - 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 αβ, but not γδ, T cells demonstrating a contribution of αβ T cells. Mice lacking either CD4+ or CD8+ T cells also had reduced mortality and mice lacking interferon (IFN)-γ were completely protected. Clearance of infectious virus was identical in mice without T cells or IFN-γ, but clearance of viral RNA was delayed compared to normal mice. Mice unable to produce antibody, perforin, Fas, TNF-α 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-γ.
AB - 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 αβ, but not γδ, T cells demonstrating a contribution of αβ T cells. Mice lacking either CD4+ or CD8+ T cells also had reduced mortality and mice lacking interferon (IFN)-γ were completely protected. Clearance of infectious virus was identical in mice without T cells or IFN-γ, but clearance of viral RNA was delayed compared to normal mice. Mice unable to produce antibody, perforin, Fas, TNF-α 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-γ.
KW - Infectious immunity-virus
KW - T lymphocytes
KW - Transgenic/knockout
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U2 - 10.1016/S0165-5728(02)00108-X
DO - 10.1016/S0165-5728(02)00108-X
M3 - Article
C2 - 12044981
AN - SCOPUS:0036273668
SN - 0165-5728
VL - 127
SP - 106
EP - 114
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 1-2
ER -