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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Role of gammadelta T cells in antibody production and recovery from SFV demyelinating disease.
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Role of gammadelta T cells in antibody production and recovery from SFV demyelinating disease.

机译：γT细胞在抗体生产和从SFV脱髓鞘疾病中恢复中的作用。

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Semliki Forest Virus (SFV) encephalomyelitis has been used to study the pathogenesis of virus-induced demyelination and serves as a model for multiple sclerosis. SFV-infection of mice invariably leads to clinical weakness accompanied by CNS inflammation, viral clearance and primary demyelination by day 21 postinfection (pi), followed by recovery and remyelination by day 35 pi. We have applied this model to the examination of the effects of gammadelta T cells in antibody production and the pathogenesis of demyelinating lesions. SFV-infection of gammadelta T cell KO mice resulted in more severe clinical signs than in wild type (WT) B6 mice. SFV-infected WT and gammadelta KO mice both cleared virus by day 10 pi and inflammation was comparable. Demyelination also appeared to be similar in both groups except that KO mice did not exhibit extensive remyelination which was seen in WT mice by day 21. SFV-infected WT mice showed widespread remyelination by day 35 pi, whereas KO mice still displayed some demyelination through day 42 pi. Both WT and KO mice developed serum antibodies to SFV. However, the reactivity of WT sera with the SFV epitope, E2 T(h) peptide, was significantly higher than in KO sera. Immunization with E2 T(h) peptide resulted in elevated antibody production to this peptide (p<0.05) and earlier remyelination (day 28 pi) in KO mice. Thus, our study has shown for the first time that immunization of SFV-infected gammadelta T cell KO mice with a viral peptide, E2 T(h) peptide led to enhanced recovery and repair of the CNS.
机译：Semliki森林病毒（SFV）脑脊髓炎已用于研究病毒诱导的脱髓鞘的发病机理，并作为多发性硬化的模型。小鼠的SFV感染总是会导致临床虚弱，并在感染后第21天（pi）出现中枢神经系统炎症，病毒清除和原发性脱髓鞘，随后在感染后第35天恢复并再次发生髓鞘化。我们已经将此模型应用于检查γδT细胞在抗体产生和脱髓鞘病变的发病机理中的作用。与野生型（WT）B6小鼠相比，伽玛δT细胞KO小鼠的SFV感染导致更严重的临床体征。被SFV感染的WT和gammadelta KO小鼠都在感染后第10天清除了病毒，并且炎症具有可比性。除KO小鼠未表现出广泛的髓鞘再生（在第21天在WT小鼠中观察到）外，两组中的脱髓鞘作用也相似。 42点WT和KO小鼠均开发了针对SFV的血清抗体。但是，WT血清与SFV表位E2 T（h）肽的反应性显着高于KO血清。在KO小鼠中，用E2 T（h）肽免疫导致该肽的抗体产量增加（p <0.05）和更早的髓鞘再生（pi 28天）。因此，我们的研究首次表明，用病毒肽E2 T（h）肽免疫SFV感染的γT细胞KO小鼠免疫，可增强CNS的恢复和修复。

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