青光眼,免疫系统 z-bo 2020-11-02 379

　　Researchers at Ruhr University Bochum (RUB) studied the role of immune response in the development of glaucoma in mice. They showed that the inflammatory process is related to the pathogenesis of the disease, and the extracellular matrix molecule Tenascin-C plays a key role as a modulator of immune response. Glaucoma is a common cause of blindness worldwide. Normally, the intraocular pressure of the patient will increase, but about 40% will remain within the normal range.

　　This collaborative research was conducted by Dr. Susanne Wiemann, Dr. Jacqueline Reinhard and Prof. Andreas Faissner from the Department of Cell Morphology and Molecular Neurobiology of RUB, and Dr. Sabrina Reinehr and Prof. Stephanie Joachim from the Experimental Eye Institute of University Eye.

　　Tenascin-C affects inflammatory immune response

　　Researchers studied mice lacking Tenascin-C and compared them with animals with this protein. In both groups of animals, they all induced autoimmune glaucoma, which is similar to human glaucoma.

　　In mice without Tenascin-C, the behavior of microglia, the immune cells of the central nervous system, is different from that of mice with Tenascin-C. Cells are less reactive and release more anti-inflammatory factors. However, in animals with Tenascin-C, microglia secrete more pro-inflammatory factors.

　　Increased retinal cell death

　　The team also observed effects on retinal ganglion cells, which transmit visual information from the eye to the brain and usually die due to glaucoma damage. Compared with mice without Tenascin-C, mice with Tenascin-C died significantly more retinal ganglion cells. In contrast to mice with Tenascin-C, the optic nerves of mice without Tenascin-C remained intact.

　　The results show that Tenascin-C plays a role in glaucoma by regulating the inflammatory process. Susanne Wiemann said: "One day, this discovery may help the diagnosis of early glaucoma."