实验性自身免疫性葡萄膜炎的免疫抑制

S R Thurau, R R Caspi, C C Chan, H L Weiner, R B Nussenblatt
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引用次数: 0

摘要

用完全弗氏佐剂中的视网膜s抗原(S-Ag)主动免疫大鼠诱导实验性自身免疫性葡萄膜炎(EAU)。相反,口服抗原可诱导特异性抑制。我们研究了口服S-Ag治疗EAU的可能性。主动免疫前,大鼠口服S-Ag 3 × 1 mg。与未治疗的对照组相比,经临床和组织学检查,治疗大鼠明显免受EAU的侵害。大鼠淋巴细胞在体外对S-Ag无增殖反应,但对其他抗原有正常的增殖反应。s - ag喂养大鼠的cd8阳性T细胞在体外抑制抗原特异性葡萄膜源性T细胞系的增殖。此外,主动免疫后再饲喂可抑制主动免疫的炎症反应强度。这些数据表明,口服给药诱导抑制,这对葡萄膜炎的发展提供了显著的保护。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Immunologic suppression of experimental autoimmune uveitis].

Experimental autoimmune uveitis (EAU) is induced in rats by active immunization with retinal S-Antigen (S-Ag) in complete Freund's adjuvant. In contrast, oral administration of an antigen induces specific suppression. We investigated the potential of oral administration of S-Ag for the treatment of EAU. Prior to active immunization rats received 3 x 1 mg S-Ag orally. In contrast to untreated controls, the treated rats were significantly protected from EAU, as determined by clinical and histological examination. Lymphocytes from treated rats showed no proliferative response to S-Ag in vitro, but had a normal proliferative response to other antigens. CD8-positive T cells from S-Ag-fed rats inhibited the proliferation of an antigen-specific uveitogenic T-cell line in vitro. Moreover, the intensity of the inflammatory reaction to active immunization could be suppressed when feeding was started after the active immunization. These data show, that oral administration induced suppression, which provided significant protection from the development of uveitis.

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