在感染小鼠肝炎病毒的小鼠中，若缺乏γ干扰素，CD4 T细胞介导的脱髓鞘作用会增强。
CD4 T-cell-mediated demyelination is increased in the absence of gamma interferon in mice infected with mouse hepatitis virus.
作者信息
Pewe Lecia, Haring Jodie, Perlman Stanley
机构信息
Department of Pediatrics, University of Iowa, Iowa City, Iowa 52242, USA.
出版信息
J Virol. 2002 Jul;76(14):7329-33. doi: 10.1128/jvi.76.14.7329-7333.2002.
Abstract
Mice infected with the murine coronavirus, mouse hepatitis virus, strain JHM (MHV) develop an immune-mediated demyelinating encephalomyelitis. Adoptive transfer of MHV-immune splenocytes depleted of either CD4 or CD8 T cells to infected mice deficient in recombination activation gene 1 resulted in demyelination. We showed previously that the process of CD8 T-cell-mediated demyelination was strongly dependent on the expression of gamma interferon (IFN-gamma) by donor cells. In this report, we show, in contrast, that demyelination and lymphocyte infiltration were increased in recipients of IFN-gamma(-/-) CD4 T cells when compared to levels in mice receiving C57BL/6 CD4 T cells.
摘要
感染鼠冠状病毒JHM株（MHV）的小鼠会发生免疫介导的脱髓鞘性脑脊髓炎。将缺失CD4或CD8 T细胞的MHV免疫脾细胞过继转移到缺乏重组激活基因1的感染小鼠中，会导致脱髓鞘。我们之前表明，CD8 T细胞介导的脱髓鞘过程强烈依赖于供体细胞中γ干扰素（IFN-γ）的表达。相比之下，在本报告中我们发现，与接受C57BL/6 CD4 T细胞的小鼠相比，接受IFN-γ（-/-）CD4 T细胞的受体小鼠的脱髓鞘和淋巴细胞浸润增加。
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