Gelderman M P, Charukamnoetkanok P, Brady J P, Hung L, Zigler J S, Wawrousek E F, Vistica B P, Fortin E, Chan C-C, Gery I
National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892-1857, USA.
Clin Exp Immunol. 2003 Aug;133(2):177-81. doi: 10.1046/j.1365-2249.2003.02218.x.
Lens-associated uveitis (LAU), a severe inflammatory eye disease, is thought to be mediated by autoimmunity against lens crystallins. Previously described animal models for this disease are antibody-mediated, since no cellular response to self crystallins could be induced in experimental animals. Here, we describe a new model for LAU, in which lymphocytes from knockout mice deficient in alphaB-crystallin are sensitized against the deleted protein and induce severe ocular inflammation when adoptively transferred into wild type recipients. Similar to LAU, the experimental disease developed only following rupture of the lens capsule, produced in this study by capsulotomy; no disease was detected in recipient eyes with no capsulotomy, or in those treated with cautery, or in eyes affected by systemic treatment with sodium iodate, lipopolysaccharide or X-irradiation. The ocular changes in affected eyes included heavy cellular infiltration and proteinaceous exudate in both the anterior and posterior segments of the eye, that reached their peak on day 4 following cell transfer and subsided quite rapidly thereafter.
晶状体相关性葡萄膜炎（LAU）是一种严重的眼部炎症性疾病，被认为是由针对晶状体晶状体蛋白的自身免疫介导的。先前描述的该疾病动物模型是抗体介导的，因为在实验动物中无法诱导对自身晶状体蛋白的细胞反应。在此，我们描述了一种新的LAU模型，其中来自缺乏αB晶状体蛋白的基因敲除小鼠的淋巴细胞对缺失的蛋白产生致敏，当将其过继转移到野生型受体中时会诱导严重的眼部炎症。与LAU相似，实验性疾病仅在本研究中通过晶状体囊切开术导致的晶状体囊破裂后才会发生；在未进行囊切开术的受体眼中、接受烧灼治疗的眼中或接受碘酸钠、脂多糖或X射线全身治疗的眼中均未检测到疾病。受影响眼睛的眼部变化包括眼前段和眼后段均有大量细胞浸润和蛋白质渗出，在细胞转移后第4天达到高峰，此后迅速消退。
