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慢性原发性闭角型青光眼患者房水中的新型炎症细胞因子 (IL-36、37、38)。

Novel inflammatory cytokines (IL-36, 37, 38) in the aqueous humor from patients with chronic primary angle closure glaucoma.

机构信息

Department of Ophthalmology, Huashan Hospital, Fudan University, Shanghai, China.

School of Public Health, Sun Yat-Sen University, Guangzhou, China.

出版信息

Int Immunopharmacol. 2019 Jun;71:164-168. doi: 10.1016/j.intimp.2019.03.016. Epub 2019 Mar 20.

DOI:10.1016/j.intimp.2019.03.016
PMID:30901679
Abstract

Glaucoma eventually leads to optic nerve damage and vision loss without medical intervention. More than 50% of glaucoma caused blindness are attributed to primary angle closure glaucoma, particularly in Asians. It is reported that immune inflammation is involved in the progress of glaucoma. Increased inflammation cytokines are detected in the aqueous humor of chronic primary angle closure glaucoma (CPACG). IL-36, IL-37 and IL-38, are novel cytokines and are involved in many inflammatory diseases, including inflammatory bowel diseases and acute anterior uveitis, but the possible contributing role in the pathogenesis of CPACG is unclear. In our current study, increased IL-36, IL-37 and IL-38 were detected in the aqueous humor of CPACG compared with age-related cataract (ARC). Furthermore, a significant correlation was detected between mean deviation of visual field (MDVF) of CPACG and IL-36, IL-37 or IL-38, respectively. Our data suggest IL-36, IL-37 and IL-38 might contribute to the immunological mediated pathogenesis of CPACG, despite the eye being an immune-privileged organ under normal conditions. The precise underlying mechanism of these cytokines during the development of CPACG remains to be explored. Our findings may be useful in therapeutic targeting of specific pathology.

摘要

青光眼最终会导致视神经损伤和视力丧失,如果没有医学干预。超过 50%的青光眼导致失明归因于原发性闭角型青光眼,特别是在亚洲人。据报道,免疫炎症参与了青光眼的进展。在慢性原发性闭角型青光眼(CPACG)的房水中检测到炎症细胞因子增加。IL-36、IL-37 和 IL-38 是新型细胞因子,参与许多炎症性疾病,包括炎症性肠病和急性前葡萄膜炎,但在 CPACG 发病机制中的可能作用尚不清楚。在我们目前的研究中,与年龄相关性白内障(ARC)相比,CPACG 的房水中检测到 IL-36、IL-37 和 IL-38 增加。此外,CPACG 的平均视野缺损(MDVF)与 IL-36、IL-37 或 IL-38 之间分别检测到显著相关性。我们的数据表明,IL-36、IL-37 和 IL-38 可能有助于 CPACG 的免疫介导发病机制,尽管在正常情况下眼睛是一个免疫特权器官。这些细胞因子在 CPACG 发展过程中的精确潜在机制仍有待探索。我们的发现可能有助于针对特定病理学的治疗靶向。

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