title: Assessment of the innate and adaptive immune system in proliferative vitreoretinopathy.
abstract: OBJECTIVE
  Proliferative vitreoretinopathy (PVR) is the leading cause of failure of surgery for rhegmatogenous retinal detachment. Although indirect evidence suggests that this disease might be autoimmune in nature, direct proof for this hypothesis is lacking. The purpose of this study was to determine in a murine model whether PVR can develop in the absence of T- or B-cell immunity.
  
  
  METHODS
  Four- to six-week-old Rag-1 gene knockout (KO) and congenic wild-type mice (WT) on the C57.Bl/6 background were studied. PVR was induced by intravitreal injection of 3 μl dispase at the concentration of 0.2 U/μl. PVR development was monitored by electroretinograms, the macroscopic observation of hemorrhage, cataract, retinal folds, and of an uneven iris, as well as the histological detection of epiretinal membranes on haematoxylin-eosin stained tissue. Additionally, immunofluorescence analysis was performed. These manifestations of PVR were assessed 1, 2, 4, 6, and 8 weeks after the intravitreal injection.
  
  
  RESULTS
  The data showed that the immune-deficient Rag-1 KO mice developed PVR with similar kinetics and severity as did the fully immune competent congenic WT mice. Carboxyfluorescein diacetate succinimidyl ester-labeled T cells that are specific for ovalbumin were detected in the inflamed vitreous and retina showing that T cells that are not specific for autoantigens present in the eye can migrate to PVR lesions. Therefore, the mere presence of T cells in PVR lesions does not imply an autoimmune pathogenesis.
  
  
  CONCLUSIONS
  This study suggests that T- and B-cell immunity is not essential for the induction of PVR.
authors.affiliation: Department of Pathology, Case Western Reserve University, Cleveland, OH, USA.
authors.forename: W
authors.initials: W
authors.lastname: Zhang
authors.forename: J
authors.initials: J
authors.lastname: Tan
authors.forename: Y
authors.initials: Y
authors.lastname: Liu
authors.forename: W
authors.initials: W
authors.lastname: Li
authors.forename: Q
authors.initials: Q
authors.lastname: Gao
authors.forename: P V
authors.initials: PV
authors.lastname: Lehmann
mesh_terms: D056704:Adaptive Immunity / Q000502:physiology*; D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology; D004195:Disease Models, Animal; D004596:Electroretinography; D005260:Female; D007113:Immunity, Innate / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008822:Mice, Transgenic; D010047:Ovalbumin / Q000276:immunology; D012160:Retina / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D018630:Vitreoretinopathy, Proliferative / Q000276:immunology* / Q000473:pathology; D014822:Vitreous Body / Q000276:immunology
chemical_list: D010047:Ovalbumin