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角膜受伤后,针对无血管晶状体的免疫反应涉及睫状带纤维。

An immune response to the avascular lens following wounding of the cornea involves ciliary zonule fibrils.

机构信息

Department of Pathology, Anatomy and Cell Biology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA.

Department of Anatomy and Cell Biology, George Washington University School of Medicine and Health Sciences, Washington, DC, USA.

出版信息

FASEB J. 2020 Jul;34(7):9316-9336. doi: 10.1096/fj.202000289R. Epub 2020 May 25.

Abstract

The lens and central cornea are avascular. It was assumed that the adult lens had no source of immune cells and that the basement membrane capsule surrounding the lens was a barrier to immune cell migration. Yet, microfibril-associated protein-1 (MAGP1)-rich ciliary zonules that originate from the vasculature-rich ciliary body and extend along the surface of the lens capsule, form a potential conduit for immune cells to the lens. In response to cornea debridement wounding, we find increased expression of MAGP1 throughout the central corneal stroma. The immune cells that populate this typically avascular region after wounding closely associate with this MAGP1-rich matrix. These results suggest that MAGP1-rich microfibrils support immune cell migration post-injury. Using this cornea wound model, we investigated whether there is an immune response to the lens following cornea injury involving the lens-associated MAGP1-rich ciliary zonules. Our results provide the first evidence that following corneal wounding immune cells are activated to travel along zonule fibers that extend anteriorly along the equatorial surface of the lens, from where they migrate across the anterior lens capsule. These results demonstrate that lens-associated ciliary zonules are directly involved in the lens immune response and suggest the ciliary body as a source of immune cells to the avascular lens.

摘要

晶状体和中央角膜是无血管的。人们曾认为,成年晶状体没有免疫细胞的来源,而环绕晶状体的基底层囊是免疫细胞迁移的屏障。然而,富含微纤维相关蛋白-1(MAGP1)的睫状带从富含血管的睫状体延伸,并沿着晶状体囊表面延伸,为免疫细胞进入晶状体提供了潜在的途径。在角膜清创性创伤后,我们发现 MAGP1 在整个中央角膜基质中的表达增加。在创伤后填充这个通常无血管区域的免疫细胞与富含 MAGP1 的基质密切相关。这些结果表明,富含 MAGP1 的微纤维支持损伤后免疫细胞的迁移。使用这种角膜创伤模型,我们研究了在涉及与 MAGP1 丰富的睫状带相关的晶状体的角膜损伤后,是否会对晶状体产生免疫反应。我们的结果首次提供了证据,表明在角膜创伤后,免疫细胞被激活,沿着从前向后延伸到晶状体赤道表面的睫状带纤维迁移,从那里它们穿过晶状体前囊。这些结果表明,与晶状体相关的睫状带直接参与了晶状体的免疫反应,并提示睫状体是无血管晶状体免疫细胞的来源。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/966e/7384020/a7817da3efca/FSB2-34-9316-g001.jpg

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