Department of Ophthalmology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo 160-8582, Japan.
Department of Internal Medicine, Division of Rheumatology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo 160-8582, Japan.
Int J Mol Sci. 2021 Oct 30;22(21):11820. doi: 10.3390/ijms222111820.
Autoimmune epithelitis and chronic inflammation are one of the characteristic features of the immune pathogenesis of Sjögren's syndrome (SS)-related dry eye disease. Autoimmune epithelitis can cause the dysfunction of the excretion of tear fluid and mucin from the lacrimal glands and conjunctival epithelia and meibum from the meibomian glands. The lacrimal gland and conjunctival epithelia express major histocompatibility complex class II or human leukocyte antigen-DR and costimulatory molecules, acting as nonprofessional antigen-presenting cells for T cell and B cell activation in SS. Ocular surface epithelium dysfunction can lead to dry eye disease in SS. Considering the mechanisms underlying SS-related dry eye disease, this review highlights autoimmune epithelitis of the ocular surface, chronic inflammation, and several other molecules in the tear film, cornea, conjunctiva, lacrimal glands, and meibomian glands that represent potential targets in the treatment of SS-related dry eye disease.
自身免疫性上皮炎和慢性炎症是干燥综合征(SS)相关干眼疾病免疫发病机制的特征之一。自身免疫性上皮炎可导致泪腺和结膜上皮以及睑板腺的泪液和黏蛋白分泌功能障碍和睑脂排出异常。泪腺和结膜上皮表达主要组织相容性复合体 II 类或人类白细胞抗原-DR 和共刺激分子,作为 SS 中 T 细胞和 B 细胞激活的非专业抗原提呈细胞。眼表面上皮功能障碍可导致 SS 中的干眼疾病。考虑到 SS 相关干眼疾病的发病机制,本综述强调了眼表面的自身免疫性上皮炎、慢性炎症以及泪膜、角膜、结膜、泪腺和睑板腺中的其他几种分子,它们是治疗 SS 相关干眼疾病的潜在靶点。