期刊
OCULAR SURFACE
卷 6, 期 3, 页码 108-116出版社
ETHIS COMMUNICATINS, INC
DOI: 10.1016/S1542-0124(12)70279-3
关键词
cornea; inflammation; keratitis; lipopolysaccharide (LPS); MyD88; Toll-like receptor
资金
- NEI NIH HHS [P30EY11373, R01EY14362, P30 EY011373, R01 EY014362] Funding Source: Medline
The Toll-like receptor (TLR) family of pathogen recognition molecules has an important role in recognizing microbial pathogens and microbial breakdown products. Activation of TLRs in the corneal epithelium induces CXC chemokine production and recruitment of neutrophils to the corneal stroma. Although essential for pathogen killing, neutrophils can cause extensive tissue damage, leading to visual impairment and blindness. In this review, we examine the role of TLRs in microbial keratitis and in noninfectious corneal inflammation, most commonly associated with contact lens wear. We present recent findings on TLR signaling pathways in the cornea, including MyD88- and TRIF-dependent responses and discuss the role of resident macrophages and dendritic cells. Finally, we examine the potential for targeting the TLR pathway as a potential therapeutic intervention for microbial keratitis and contact lens-associated corneal inflammation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据