Th17 cells have been implicated in the pathogenesis of numerous inflammatory and autoimmune conditions. At the ocular surface, Th17 cells have been identified as key effector cells in chronic ocular surface disease. Evidence from murine studies indicates that following differentiation and expansion, Th17 cells migrate from the lymphoid tissues to the eye, where they release inflammatory cytokines including, but not limited to, their hallmark cytokine IL-17A. As the acute phase subsides, a population of long-lived memory Th17 cells persist, which predispose hosts both to chronic inflammation and severe exacerbations of disease; of great interest is the small subset of Th17/1 cells that secrete both IL-17A and IFN-γ in acute-on-chronic disease exacerbation. Over the past decade, substantial progress has been made in deciphering how Th17 cells interact with the immune and neuroimmune pathways that mediate chronic ocular surface disease. Here, we review (i) the evidence for Th17 immunity in chronic ocular surface disease, (ii) regulatory mechanisms that constrain the Th17 immune response, and (iii) novel therapeutic strategies targeting Th17 cells.

Th17 细胞与许多炎症和自身免疫病的发病机制有关。在眼表，Th17 细胞已被确定为慢性眼表疾病的关键效应细胞。来自小鼠研究的证据表明，在分化和扩增后，Th17 细胞从淋巴组织迁移到眼睛，在那里它们释放炎性细胞因子，包括但不限于它们的标志性细胞因子 IL-17A。随着急性期的消退，长期存在的记忆 Th17 细胞群持续存在，这使宿主易患慢性炎症和疾病的严重恶化；令人感兴趣的是在急性慢性疾病恶化中分泌 IL-17A 和 IFN-γ 的一小部分 Th17/1 细胞。在过去的十年，在破译 Th17 细胞如何与介导慢性眼表疾病的免疫和神经免疫通路相互作用方面取得了实质性进展。在这里，我们回顾了 (i) Th17 免疫在慢性眼表疾病中的证据，(ii) 限制 Th17 免疫反应的调节机制，以及 (iii) 针对 Th17 细胞的新治疗策略。