title: Soluble TNF receptors in vitreoretinal proliferative disease.
abstract: OBJECTIVE
  To measure vitreous levels of soluble TNF-receptors (sTNF-Rs) types I and II in eyes with rhegmatogenous retinal detachment (RRD), uncomplicated or complicated with proliferative vitreoretinopathy (PVR), and in eyes with proliferative diabetic retinopathy (PDR). To examine whether there is any relationship between vitreous levels of sTNF-Rs and clinical features of these conditions and between vitreous sTNF-Rs and TNFalpha levels and serum levels of sTNF-RS:
  
  
  METHODS
  Vitreous levels of sTNF-Rs and TNFalpha were measured by enzyme-linked immunosorbent assay in 30 eyes with PVR, 30 eyes with uncomplicated RRD, and 29 eyes with PDR. Vitreous from eyes of 10 deceased donors and 9 eyes with macular holes served as control specimens. Serum levels of sTNF-Rs were measured in 17 patients with PDR and 21 patients with PVR.
  
  
  RESULTS
  Vitreous levels of sTNF-Rs I and II were increased in eyes with PVR, RRD, and PDR when compared with control eyes (P < 0.002). However, vitreous levels of sTNF-Rs I and II were higher in eyes with PVR than in eyes with RRD (P < 0.01) or PDR (P < 0.03). This contrasted with the findings that serum sTNF-Rs were higher in PDR than in PVR (P < 0.016) and that vitreous levels of TNFalpha were higher in eyes with PDR than in eyes with PVR (P < 0.0005). In PVR, vitreous sTNF-Rs levels were associated with the duration of retinal detachment, number of previous external operations, and grade of severity, whereas in PDR these levels were not related to the type or duration of diabetes or its complication with traction retinal detachment.
  
  
  CONCLUSIONS
  These observations suggest the existence of TNF inhibitory mechanisms within the eye during retinal processes of inflammation and angiogenesis. That high vitreous levels of sTNF-Rs relate to severity of retinopathy suggests that these molecules may constitute reactive products of inflammation. Effective control of TNFalpha activity by sTNF-Rs within the retinal microenvironment may determine the outcome and severity of retinal proliferative conditions.
authors.affiliation: Institute of Ophthalmology and Moorfields Eye Hospital, London, United Kingdom. g.limb@ucl.ac.uk
authors.forename: G A
authors.initials: GA
authors.lastname: Limb
authors.forename: R D
authors.initials: RD
authors.lastname: Hollifield
authors.forename: L
authors.initials: L
authors.lastname: Webster
authors.forename: D G
authors.initials: DG
authors.lastname: Charteris
authors.forename: A H
authors.initials: AH
authors.lastname: Chignell
mesh_terms: D003930:Diabetic Retinopathy / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism*; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism*; D012163:Retinal Detachment / Q000378:metabolism*; D012167:Retinal Perforations / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D018630:Vitreoretinopathy, Proliferative / Q000378:metabolism*; D014822:Vitreous Body / Q000378:metabolism*
chemical_list: D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000068800:Etanercept