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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Accelerated induction of experimental allergic encephalomyelitis in PL/J mice by a non-V beta 8-specific superantigen.
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Accelerated induction of experimental allergic encephalomyelitis in PL/J mice by a non-V beta 8-specific superantigen.

机译：非Vβ8特异性超抗原加速PL / J小鼠实验性变应性脑脊髓炎的诱导。

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Superantigens such as the staphylococcal enterotoxins can play an important role in exacerbation of autoimmune disorders such as experimental allergic encephalomyelitis (EAE) in mice. In fact, superantigens can reactivate EAE in PL/J mice that have been sensitized to rat myelin basic protein (MBP). The T-cell subset predominantly responsible for disease in PL/J mice bears the V beta 8+ T-cell antigen receptor (TCR). The question arises as to whether T cells bearing other V beta specificities are involved in induction or reactivation of EAE with superantigen. Thus, we have investigated the ability of a non-V beta 8-specific superantigen, staphylococcal enterotoxin A (SEA) (V beta specificities 1, 3, 10, 11, and 17), to induce EAE in PL/J mice that have been previously protected from disease by anergy and deletion of V beta 8+ T cells. PL/J mice were first pretreated with the V beta 8-specific superantigen staphylococcal enterotoxin B (SEB) and then immunized with MBP. These mice exhibited V beta 8-specific anergy and depletion and did not develop EAE, even when further treated with SEB. However, administration of SEA to these same mice induced an initial episode of EAE which was characterized by severe hindleg paralysis and accelerated onset of disease. In contrast to SEB pretreatment, PL/J mice pretreated with SEA did develop EAE when immunized with MBP, and after resolution of clinical signs of disease these mice were susceptible to relapse of EAE induced by SEB but not by SEA. Thus, superantigens can activate encephalitogenic MBP-specific non-V beta 8+ T cells to cause EAE in PL/J mice. These data suggest that superantigens can play a central role in autoimmune disorders and that they introduce a profound complexity to autoimmune diseases such as EAE, akin to the complexity seen in multiple sclerosis.
机译：超抗原（例如葡萄球菌肠毒素）在加重自身免疫性疾病（例如小鼠实验性过敏性脑脊髓炎（EAE））中起重要作用。实际上，超抗原可以在已经对大鼠髓鞘碱性蛋白（MBP）致敏的PL / J小鼠中重新激活EAE。在PL / J小鼠中主要负责疾病的T细胞亚群具有V beta 8+ T细胞抗原受体（TCR）。出现有关带有其他Vβ特异性的T细胞是否参与超抗原诱导或再激活EAE的问题。因此，我们研究了非Vβ8特异性超抗原葡萄球菌肠毒素A（SEA）（Vβ特异性1、3、10、11和17）在PL / J小鼠中诱发EAE的能力。以前已经通过无反应性和V beta 8+ T细胞的缺失保护了自己免受疾病侵袭。首先用V beta 8特异性超抗原葡萄球菌肠毒素B（SEB）预处理PL / J小鼠，然后用MBP免疫。这些小鼠表现出V beta 8特异性无能和耗竭，甚至用SEB进一步治疗时也没有发展出EAE。然而，向这些相同的小鼠施用SEA诱导了EAE的初始发作，其特征在于严重的后腿麻痹和疾病的加速发作。与SEB预处理相比，用SEA预处理的PL / J小鼠在用MBP免疫时确实会发展成EAE，在疾病的临床症状消失后，这些小鼠易受SEB诱导而不是SEA诱导的EAE复发。因此，超抗原可以激活致脑病的MBP特异性非Vβ8+ T细胞，从而在PL / J小鼠中引起EAE。这些数据表明，超抗原可以在自身免疫性疾病中发挥重要作用，并且它们为诸如EAE的自身免疫性疾病带来了深远的复杂性，类似于多发性硬化症中所见的复杂性。

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