title: How herpes simplex virus type 1 rescinds corneal privilege.
abstract: Properties of the cornea such as a lack of blood and lymphatic vessels, a lack of professional antigen-presenting cells, and exposure to immunosuppressive factors in the aqueous humor contribute to a relative state of immune privilege. Ironically, corneal damage and the accompanying visual morbidity following herpes simplex virus type 1 (HSV-1) infection does not results from uncontrolled viral replication, but from an immunoinflammatory process referred to as herpes stromal keratitis (HSK). This review highlights changes in the immune-privileged status of the cornea following HSV-1 infection that contribute to HSK.
authors.affiliation: Departments of Immunology, School of Medicine, University of Pittsburgh, Pittsburgh, Pa., USA.
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Lepisto
authors.forename: Gregory M
authors.initials: GM
authors.lastname: Frank
authors.forename: Robert L
authors.initials: RL
authors.lastname: Hendricks
mesh_terms: D000818:Animals; D017951:Antigen Presentation; D015496:CD4-Positive T-Lymphocytes / Q000502:physiology; D003315:Cornea / Q000276:immunology*; D016207:Cytokines / Q000502:physiology; D004195:Disease Models, Animal; D018259:Herpesvirus 1, Human; D006801:Humans; D007108:Immune Tolerance; D016849:Keratitis, Herpetic / Q000276:immunology*; D018919:Neovascularization, Physiologic
chemical_list: D016207:Cytokines