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视网膜光感受器抗原与脾细胞偶联对实验性自身免疫性葡萄膜炎的抑制作用

Inhibition of experimental autoimmune uveitis by retinal photoreceptor antigens coupled to spleen cells.

作者信息

Dua H S, Gregerson D S, Donoso L A

机构信息

Retina Service, Wills Eye Hospital, Philadelphia, Pennsylvania 19107.

出版信息

Cell Immunol. 1992 Feb;139(2):292-305. doi: 10.1016/0008-8749(92)90072-w.

Abstract

Experimental autoimmune uveitis (EAU) and experimental autoimmune pinealitis (EAP) are CD4+ T cell-mediated inflammatory diseases of the uveal tract and retina of the eye and of the pineal gland. EAU and EAP can be induced by several retinal autoantigens including S-antigen (S-Ag) and interphotoreceptor retinoid binding protein (IRBP). In this study we investigated the effect of intravenous administration of S-Ag and IRBP coupled to syngeneic spleen cells on the development of EAU and EAP. Injection of S-Ag or IRBP coupled to spleen cells 5 days prior to immunization with native S-Ag or IRBP, respectively, was effective in preventing the induction of EAU and EAP in LEW rats. Conversely, LEW rats receiving S-Ag-coupled spleen cells and challenged with IRBP or LEW rats receiving IRBP-coupled spleen cells and challenged with S-Ag developed a severe EAU within 10 days to 2 weeks following immunization, as did all control animals receiving sham-coupled spleen cells and challenged with the two retinal antigens. The results show that the administration of retinal autoantigens coupled to spleen cells effectively protects against the development of EAU when animals are subsequently challenged with the tolerizing antigen but not when challenged with another unrelated pathogenic retinal autoantigen.

摘要

实验性自身免疫性葡萄膜炎(EAU)和实验性自身免疫性松果体炎(EAP)是由CD4 + T细胞介导的眼部葡萄膜和视网膜以及松果体的炎症性疾病。EAU和EAP可由多种视网膜自身抗原诱导,包括S抗原(S-Ag)和光感受器间类视黄醇结合蛋白(IRBP)。在本研究中,我们调查了静脉注射与同基因脾细胞偶联的S-Ag和IRBP对EAU和EAP发展的影响。分别在用天然S-Ag或IRBP免疫前5天注射与脾细胞偶联的S-Ag或IRBP,可有效预防LEW大鼠中EAU和EAP的诱导。相反,接受S-Ag偶联脾细胞并用IRBP攻击的LEW大鼠,或接受IRBP偶联脾细胞并用S-Ag攻击的LEW大鼠,在免疫后10天至2周内出现严重的EAU,所有接受假偶联脾细胞并用两种视网膜抗原攻击的对照动物也是如此。结果表明,当动物随后用耐受抗原攻击时,与脾细胞偶联的视网膜自身抗原的给药可有效预防EAU的发展,但当用另一种无关的致病性视网膜自身抗原攻击时则不然。

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