Cirone Mara, Cuomo Laura, Zompetta Claudia, Ruggieri Stefano, Frati Luigi, Faggioni Alberto, Ragona Giuseppe
Dipartimento di Medicina Sperimentale e Patologia, Università La Sapienza, Roma, Italy.
J Med Virol. 2002 Oct;68(2):268-72. doi: 10.1002/jmv.10190.
Several reports have suggested an association of human herpesvirus 6 (HHV-6) with multiple sclerosis. Autoreactive T lymphocytes directed against myelin components seem to contribute to the pathogenesis of the disease. It has been suggested that molecular mimicry between viral and self-antigens might be one of the mechanisms that determine the onset of several autoimmune diseases. Following this hypothesis, the purpose of the present study was to evaluate if HHV-6 could play a role in activating T cells capable of cross-reaction with an important myelin component, the myelin basic protein. T cell lines were established from 22 multiple sclerosis patients and from 16 healthy controls, and their capability to react to both virus and myelin basic protein antigens was compared. The analysis of T cell cross-reactivity in patients and controls did not show significant differences in the HHV-6 ability to activate myelin basic protein-reactive T cells. Similarly, the evaluation of the humoral immune response to HHV-6 in patients and controls did not mirror any abnormality in the HHV-6 status in multiple sclerosis patients. Therefore, although the findings of activity in vitro of T cell lines with dual specificity are consistent with the hypothesis of molecular mimicry, the lack of differences in cross-reactivity between patients and controls do not support molecular mimicry as an important mechanism in the physiopathology of this disease.
几份报告表明人类疱疹病毒6型（HHV - 6）与多发性硬化症有关联。针对髓鞘成分的自身反应性T淋巴细胞似乎在该疾病的发病机制中起作用。有人提出病毒抗原与自身抗原之间的分子模拟可能是决定几种自身免疫性疾病发病的机制之一。基于这一假设，本研究的目的是评估HHV - 6是否能在激活能够与一种重要的髓鞘成分——髓鞘碱性蛋白发生交叉反应的T细胞中发挥作用。从22例多发性硬化症患者和16名健康对照者中建立T细胞系，并比较它们对病毒和髓鞘碱性蛋白抗原的反应能力。对患者和对照者T细胞交叉反应性的分析未显示HHV - 6激活髓鞘碱性蛋白反应性T细胞的能力有显著差异。同样，对患者和对照者针对HHV - 6的体液免疫反应的评估也未反映出多发性硬化症患者HHV - 6状态有任何异常。因此，尽管具有双重特异性的T细胞系体外活性的研究结果与分子模拟假说一致，但患者和对照者在交叉反应性方面缺乏差异并不支持分子模拟是该疾病生理病理学中的一个重要机制。
