Bowern N, Ramshaw I A, Clark I A, Doherty P C
J Exp Med. 1984 Nov 1;160(5):1532-43. doi: 10.1084/jem.160.5.1532.
Lewis rats that are primed with guinea pig spinal cord homogenized in complete Freund's adjuvant (GPSCH-CFA) develop overt symptoms of experimental allergic encephalomyelitis (EAE). Treatment with the iron-chelating agent, desferrioxamine B mesylate (DFOM), at various times before the onset of EAE, dramatically suppressed both the severity and duration of disease. When DFOM was administered to rats soon after the development of neurological signs, a rapid recovery occurred, though mild, transient symptoms could be seen approximately 1 wk after withdrawal of the drug. Treatment with DFOM was always accompanied by a diminution of T cell responsiveness on the part of the delayed-type hypersensitivity/helper subset and, on histological examination, an absence of inflammatory cells from lesions. Iron is believed to influence both the migration and function of immune effector cells. It can also act as a catalyst in the formation of free radicals, which are highly toxic agents causing tissue damage in sites of inflammation. The mechanisms underlying the effect of DFOM on the severity of EAE, and the possible implications for treatment of multiple sclerosis are discussed.
用完全弗氏佐剂（CFA）乳化的豚鼠脊髓匀浆（GPSCH）致敏的刘易斯大鼠会出现明显的实验性自身免疫性脑脊髓炎（EAE）症状。在EAE发病前的不同时间用铁螯合剂甲磺酸去铁胺（DFOM）进行治疗，可显著减轻疾病的严重程度和持续时间。当在神经症状出现后不久给大鼠施用DFOM时，会迅速恢复，尽管在停药后约1周可能会出现轻微、短暂的症状。DFOM治疗总是伴随着迟发型超敏反应/辅助亚群的T细胞反应性降低，并且在组织学检查中，病变部位没有炎性细胞。铁被认为会影响免疫效应细胞的迁移和功能。它还可以作为自由基形成的催化剂，自由基是导致炎症部位组织损伤的高毒性物质。本文讨论了DFOM对EAE严重程度影响的潜在机制以及对多发性硬化症治疗的可能意义。
