Uhlig T, Cooper D, Eber E, McMenamin C, Wildhaber J H, Sly P D
Division of Clinical Sciences, TVW Telethon Institute for Child Health Research, West Perth, Western Australia.
Clin Exp Allergy. 1998 Jun;28(6):758-64. doi: 10.1046/j.1365-2222.1998.00309.x.
Short-term treatment with leflunomide is effective in suppressing antigen-specific antibody production and allergen-induced bronchoconstriction after sensitization. This agent may thus have a role in future primary prevention strategies in allergic disease.
The current study aimed to determine whether long-term oral treatment with leflunomide prevents allergic sensitization permanently.
After sensitization with ovalbumin, six groups of rats (n = 31) were treated daily with leflunomide or diluent for up to 30 days. Ovalbumin-specific IgE and IgG were determined weekly for at least 2 weeks after cessation of treatment. T lymphocytes from another 21 animals were stimulated ex vivo with ovalbumin or concanavalin A.
Ovalbumin-specific IgE and IgG were lower during treatment with leflunomide compared with controls (P < 0.002) but increased after the cessation of treatment. Antigen-specific T-cell proliferation was decreased in cells obtained from leflunomide treated animals (P < 0.05), but not when stimulated with concanavalin A. Eosinophil (P < 0.0001) and neutrophil (P < 0.02) numbers in bronchoalveolar lavage 24 h after allergen challenge were lower in the leflunomide treated animals.
Leflunomide prevents antigen-specific immunoglobulin production after sensitization during treatment, inhibits allergen-induced airway inflammation and diminishes antigen-specific T lymphocyte proliferation.
来氟米特短期治疗可有效抑制致敏后抗原特异性抗体产生及变应原诱导的支气管收缩。因此，该药物可能在未来过敏性疾病的一级预防策略中发挥作用。
本研究旨在确定来氟米特长期口服治疗是否能永久性预防过敏致敏。
用卵清蛋白致敏后，六组大鼠（n = 31）每天接受来氟米特或稀释剂治疗，持续30天。在治疗停止后至少2周内，每周测定卵清蛋白特异性IgE和IgG。另外21只动物的T淋巴细胞在体外分别用卵清蛋白或伴刀豆球蛋白A刺激。
与对照组相比，来氟米特治疗期间卵清蛋白特异性IgE和IgG较低（P < 0.002），但治疗停止后升高。来氟米特治疗动物的细胞中抗原特异性T细胞增殖减少（P < 0.05），但用伴刀豆球蛋白A刺激时未减少。在变应原激发后24小时，来氟米特治疗动物支气管肺泡灌洗中的嗜酸性粒细胞（P < 0.0001）和中性粒细胞（P < 0.02）数量较低。
来氟米特在治疗期间可预防致敏后抗原特异性免疫球蛋白产生，抑制变应原诱导的气道炎症，并减少抗原特异性T淋巴细胞增殖。
