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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 >Synthetic peptides fail to induce nasal tolerance to experimental autoimmune myasthenia gravis.
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Synthetic peptides fail to induce nasal tolerance to experimental autoimmune myasthenia gravis.

机译：合成肽不能诱导对实验性自身免疫性重症肌无力的鼻耐受。

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摘要

Nasal administration of Torpedo acetylcholine receptor (AChR) to Lewis rats prior to induction of experimental autoimmune myasthenia gravis (EAMG) is highly efficient in prevention of clinical weakness, and suppression of AChR-specific T and B cell responses. To identify possible antigenic determinants within the receptor which can modulate EAMG and anti-AChR response, we evaluated the effects of nasal administration of alpha 61-76, alpha 100-116, alpha 146-162, delta 354-367, and alpha 261-277 of Torpedo AChR at different doses on the tolerance induction against EAMG irrespective if given at lower, the same or higher doses than whole Torpedo AChR protein, that was confirmed to be highly efficient as tolerogen to EAMG. None of these peptides, neither administrated alone nor in combination, induced tolerance to EAMG. Peptide administration did not affect the levels or affinities of anti-AChR antibodies when compared with non-tolerized control EAMG rats, while administration of whole AChR protein affected both variables. The results may indicate that the T and B cell heterogeneity of AChR epitopes makes it difficult to induce tolerance using synthetic peptide.
机译：在诱导实验性自身免疫性重症肌无力（EAMG）之前，对Lewis大鼠进行鼻鱼雷乙酰胆碱受体（AChR）鼻腔给药可有效预防临床虚弱，并抑制AChR特异性T和B细胞反应。为了确定受体中可能调节EAMG和抗AChR应答的抗原决定簇，我们评估了鼻腔给药alpha 61-76，alpha 100-116，alpha 146-162，delta 354-367和alpha 261-的效果277鱼雷AChR在不同剂量下对EAMG的耐受性诱导，无论是否以比整个鱼雷AChR蛋白更低，相同或更高的剂量给药，已确认是对EAMG的高效致耐受剂。这些肽，既不单独也不联合给药，都没有诱导出对EAMG的耐受性。与未耐受的对照EAMG大鼠相比，给予肽不会影响抗AChR抗体的水平或亲和力，而给予完整的AChR蛋白则会影响这两个变量。结果可能表明，AChR表位的T细胞和B细胞异质性使其难以诱导使用合成肽的耐受性。

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