CHARACTERIZATION OF IMMUNE RESPONSES TO RETINAL SPECIFIC ANTIGENS

S抗原(S抗原)和光感受器相互作用的特点之一 视黄醇结合蛋白(IRBP)是一种视网膜特异性抗原，是 在眼部引起强烈的自身免疫性炎症的能力 在佐剂存在的情况下注射的实验动物。这 这种疾病被称为实验性自身免疫性葡萄膜炎(EAU)，严重依赖于 T T细胞与适当的抗原提呈细胞对抗原的处理 (APCS)。抗原处理，这发生在内吞胞囊泡内 APC导致产生小的多肽亚基。这些 然后必须保护小分子多肽不被进一步降解，并 被运送到与T细胞相互作用的细胞表面 地点。 在1994财年，我们进一步鉴定了细胞内蛋白的首次鉴定 D 在1993财年。我们确认该蛋白质确实属于热休克 通过对70kD峰的部分氨基酸序列进行蛋白质家族的测定。我们 在40kD处的峰也被鉴定为肌动蛋白。使用不同的测试 多肽部分研究表明，HSP70与免疫原肽的结合 是一个有选择性的过程。某些多肽可以很好地与HSP70结合，尽管其他 多肽对HSP70没有亲和力。这个过程也是有选择性的，因为 它需要三磷酸腺苷才能释放结合肽。我们还发现了 白塞病患者血清热休克蛋白抗体水平升高 疾病。血清水平的升高与眼期相对应。 在没有任何证据表明全身活动活跃的情况下的炎症活动 疾病。

One of the characteristics of S-antigen (S-Ag) and interphotoreceptor retinoid-binding protein (IRBP), which are retinal-specific antigens, is th ability to induce an intense autoimmune inflammation in the eyes of experimental animals when injected in the presence of an adjuvant. This disease, called experimental autoimmune uveitis (EAU), is critically depend t on T cells and antigen processing by appropriate antigen-presenting cells (APCs). Antigen processing, which occurs within the endocytic vesicles of the APCs, results in the production of small polypeptide subunits. These small polypeptides must then be protected from further degradation and transported to the cell surface where the interaction with the T cell takes place. In FY 1994 we further characterized the intracellular protein first identif d in FY 1993. We confirmed that the protein does belong to the heat shock family of proteins by partial amino acid sequencing of the 70kD peak. We also identified the peak at 40kD as being actin. Testing with different peptide moieties has shown that binding of immunogenic peptides by hsp70 is a selective process. Certain peptides bind well to hsp70, although othe peptides have no affinity for hsp70. The process is also selective in that it requires ATP in order to release the bound peptide. We have also found increased levels of hsp antibody in the serum of patients with Behcet's disease. The increase serum levels corresponded to periods of ocular inflammatory activity in the absence of any evidence of active systemic disease.