Edelsten C, D'Cruz D P
Ipswich Hospital, Suffolk, UK.
Clin Rev Allergy Immunol. 1997 Spring;15(1):41-52. doi: 10.1007/BF02828276.
AECAs have been found in 26% of patients with uveoretinitis in studies arising from three different laboratories, and their presence cannot simply be explained by coexisting extraocular disease. There is little correlation with ocular disease activity or other markers of systemic inflammation and vascular damage that can be found in this group of patients, but this lack of correlation has also been found in studies of more widespread inflammatory diseases. The changes found in the peripheral blood of patients with uveoretinitis are the result of a mixture of acute and chronic inflammation, reactions to coexisting tissue damage, as well as predisposing abnormalities of inflammation and hemostasis. Even patients with similar clinical appearances are unlikely to be pathologically homogeneous, and the reasons for the presence of AECA are likely to be various. Some patients may demonstrate a heightened antibody response to endothelium damaged by unknown mechanisms, whereas others may develop cytotoxic AECA as an integral part of the inflammatory process. The majority of serum samples with AECA demonstrated antibody-dependent cell-mediated cytotoxicity, but this potentially pathogenetic mechanism was only demonstrable in a minority of patients. It is unlikely that IgM AECA or complement-mediated cytotoxicity is a relevant mechanism of vascular damage in this group of patients. A subgroup of patients may be genetically predisposed to produce excess autoantibodies in response to tissue damage caused by a wide variety of insults. Sawyerr et al.(36) has suggested that increased serum levels of agalactosyl IgG may account for some of the AECA binding found in chronic inflammatory diseases: we have also found changes in agalactosyl IgG in patients with active isolated uveoretinitis (40), but levels did not correlate with levels of IgG AECA (unpublished results). Further longitudinal studies will be necessary on each subgroup of patients in order to determine the true clinical significance of these findings.
在来自三个不同实验室的研究中，26%的葡萄膜视网膜炎患者体内发现了抗内皮细胞抗体（AECAs），其存在不能简单地用并存的眼外疾病来解释。它与眼部疾病活动或该组患者中可发现的全身炎症和血管损伤的其他标志物几乎没有相关性，但在更广泛的炎症性疾病研究中也发现了这种缺乏相关性的情况。葡萄膜视网膜炎患者外周血中发现的变化是急性和慢性炎症、对并存组织损伤的反应以及炎症和止血的易患异常混合作用的结果。即使临床表现相似的患者在病理上也不太可能是同质的，AECAs存在的原因可能多种多样。一些患者可能对由未知机制损伤的内皮细胞表现出增强的抗体反应，而另一些患者可能产生细胞毒性AECAs作为炎症过程的一个组成部分。大多数含有AECAs的血清样本表现出抗体依赖性细胞介导的细胞毒性，但这种潜在的致病机制仅在少数患者中得到证实。IgM AECAs或补体介导的细胞毒性不太可能是该组患者血管损伤的相关机制。一部分患者可能在遗传上易倾向于因各种损伤导致的组织损伤而产生过量自身抗体。索耶尔等人（36）提出，血清中去半乳糖基IgG水平升高可能解释了在慢性炎症性疾病中发现的一些AECAs结合现象：我们在活动性孤立性葡萄膜视网膜炎患者中也发现了去半乳糖基IgG的变化（40），但水平与IgG AECAs水平无关（未发表结果）。有必要对每个患者亚组进行进一步的纵向研究以确定这些发现的真正临床意义。
