期刊
JOURNAL OF NEUROINFLAMMATION
卷 20, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s12974-023-02710-3
关键词
Cornea; Interleukin 6; Myeloid cell; Nerve; Neutrophil; Toll-like receptor 2
The depletion of CD11b(hi)Ly6G(hi) or CD11b(hi)Ly6C(hi)Ly6G(lo) cells aggravates corneal nerve loss in response to sterile corneal injury, while IL-6 neutralization preserves corneal nerves and reduces myeloid cell recruitment. The TLR2-IL-6 axis drives corneal nerve loss, and corneal stromal fibroblasts are involved in this process.
BackgroundMounting evidence suggests that the immune system plays detrimental or protective roles in nerve injury and repair.Main bodyHerein we report that both CD11b(hi)Ly6G(hi) and CD11b(hi)Ly6C(hi)Ly6G(lo) myeloid cells are required to protect corneal nerves against sterile corneal injury. Selective depletion of CD11b(hi)Ly6G(hi) or CD11b(hi)Ly6C(hi)Ly6G(lo) cells resulted in aggravation of corneal nerve loss, which correlated with IL-6 upregulation. IL-6 neutralization preserved corneal nerves while reducing myeloid cell recruitment. IL-6 replenishment exacerbated corneal nerve damage while recruiting more myeloid cells. In mice lacking Toll-like receptor 2 (TLR2), the levels of IL-6 and myeloid cells were decreased and corneal nerve loss attenuated, as compared to wild-type and TLR4 knockout mice. Corneal stromal fibroblasts expressed TLR2 and produced IL-6 in response to TLR2 stimulation.ConclusionCollectively, our data suggest that CD11b(hi)Ly6G(hi) and CD11b(hi)Ly6C(hi)Ly6G(lo) myeloid cells confer corneal nerve protection under sterile injury by creating a negative-feedback loop to suppress the upstream TLR2-IL-6 axis that drives corneal nerve loss.
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