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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 >Therapy with antibody against leukocyte integrin VLA-4 (CD49d) is effective and safe in virus-facilitated experimental allergic encephalomyelitis.
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Therapy with antibody against leukocyte integrin VLA-4 (CD49d) is effective and safe in virus-facilitated experimental allergic encephalomyelitis.

机译：抗白细胞整合素VLA-4（CD49d）抗体的治疗在病毒促进的实验性变应性脑脊髓炎中有效且安全。

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摘要

Experimental allergic encephalomyelitis (EAE) is facilitated in resistant BALB/c mice by intraperitoneal infection with an avirulent Semliki Forest virus (SFV-A7). Viral infection increases the incidence of EAE from 15-30% to 60-90% and speeds up appearance of paralysis from 24 to 14 days. In this paper, we describe treatment of virus-facilitated EAE with monoclonal antibodies (mAbs) against leukocyte and/or endothelial cell adhesion molecules. Therapy with mAb against ICAM-1 (intercellular adhesion molecule-1) had a modest effect, but caused hemorrhagic brain and spinal cord lesions. Therapy with mAb against Mac-1 (alpha M beta 2-integrin) was well tolerated but had no effect. Therapy with mAb against VLA-4 (alpha 4 beta 1-integrin) was safe, diminished both clinical and histopathological signs of EAE, decreased induction of VCAM-1 (vascular cell adhesion molecule-1) on brain vessels and diminished infiltration of VLA-4+ cells into the brain. The amount of viral antigen in the brain was not altered. We conclude that facilitation of leukocyte entry into the brain is a major mechanism for viral facilitation of EAE in the BALB/c mouse, and that facilitation can be inhibited by anti-adhesion therapy. This may have implications for treatment of relapses triggered by viral infections in multiple sclerosis.
机译：通过用无毒的Semliki Forest病毒（SFV-A7）腹腔感染在耐药的BALB / c小鼠中促进实验性变应性脑脊髓炎（EAE）。病毒感染会将EAE的发生率从15-30％增加到60-90％，并将麻痹的出现速度从24天提高到14天。在本文中，我们描述了针对白细胞和/或内皮细胞粘附分子的单克隆抗体（mAb）对病毒促成的EAE的治疗。用抗ICAM-1（细胞间粘附分子-1）的mAb进行治疗的效果不明显，但会引起出血性脑部和脊髓损伤。用抗Mac-1的mAb（αMβ2-整联蛋白）进行治疗的耐受性良好，但没有效果。用抗VLA-4（alpha 4 beta 1-integrin）的mAb进行治疗是安全的，可减少EAE的临床和组织病理学迹象，减少对脑血管的VCAM-1（血管细胞粘附分子-1）的诱导，并减少VLA- 4+细胞进入大脑。脑中病毒抗原的量没有改变。我们得出的结论是，促进白细胞进入大脑是BALB / c小鼠中病毒促进EAE的主要机制，并且可以通过抗粘连疗法抑制这种促进作用。这可能对治疗由多发性硬化症中的病毒感染引发的复发具有影响。

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