Progress Of Research On Immunology Of Glaucoma

Glaucoma is defined as a group of neurodegenerative diseases expressed as characteristic atrophy of optic nerve,which ultimately result in the loss of visual field.This appearance is direct show of axonal degeneration of ganglion cells.The final death way of damaged retinal ganglion cells is apoptosis.For the past thirty years,many scholars researched pathogenesis of glaucoma in immunology,and there is great progress.Studies in the molecule immunology found that the antibodies,which lie in serum or ocular tissues,to anti-opticus were significant higher than healthy adult;HLA complex may be also concerned with immunologic development of glaucoma;Abnormal expression of cytokine could induce confused immunoloregulation.Studies in the cell immunology found that T-cell could be protective and damaged in glaucoma;Red cell immunology played a role in hemodynamics of glaucomatous patient.Glial cells played a role of immumoloregulation in the death of RGCs in glaucoma.At the same time,studies in immunology for searching treatment measures also have get great progress.Specific immunity,vaccination for example,had been used in the experiment of optic nerve protection.And nonspecific immunity,such as antagon of glutamate,calcium ion channel blocker,antioxidant and inhibitor of apoptosis and so on,have a certainly role for reducing lost of RGCs in glaucoma.Other therapeutics,for example of heat shock protein,traditional Chinese drug,mental intervention and so on,would be positive in glaucomatous optic nerve protecting.The development of glaucoma is the common result of multiple factor,but the pathogenesis is not clear completely up to now.The research of immunology offer us a new way.The humoral immunity and cellular immunity play the role of immunoloregulation in glaucoma.Based on these researches,immunologic preparation is expected to become the important way for protecting optic nerve of glaucoma in clinic.This article reviews the progress of research on immunology of glaucoma.