April 1998
Volume 39, Issue 5
Free
Articles  |   April 1998
T cell traffic and the inflammatory response in experimental autoimmune uveoretinitis.
Author Affiliations
  • R A Prendergast
    Johns Hopkins University, Baltimore, Maryland, USA.
  • C E Iliff
    Johns Hopkins University, Baltimore, Maryland, USA.
  • N M Coskuncan
    Johns Hopkins University, Baltimore, Maryland, USA.
  • R R Caspi
    Johns Hopkins University, Baltimore, Maryland, USA.
  • G Sartani
    Johns Hopkins University, Baltimore, Maryland, USA.
  • T K Tarrant
    Johns Hopkins University, Baltimore, Maryland, USA.
  • G A Lutty
    Johns Hopkins University, Baltimore, Maryland, USA.
  • D S McLeod
    Johns Hopkins University, Baltimore, Maryland, USA.
Investigative Ophthalmology & Visual Science April 1998, Vol.39, 754-762. doi:
  • Views
  • PDF
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      R A Prendergast, C E Iliff, N M Coskuncan, R R Caspi, G Sartani, T K Tarrant, G A Lutty, D S McLeod; T cell traffic and the inflammatory response in experimental autoimmune uveoretinitis.. Invest. Ophthalmol. Vis. Sci. 1998;39(5):754-762.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

PURPOSE: To quantify S-antigen-specific (S-Ag) T cells in the retina after adoptive transfer, and to evaluate their role in the initiation and progress of destructive ocular inflammation in experimental autoimmune uveoretinitis (EAU). METHODS: Lewis rats were administered 10 x 10(6) S-Ag-specific T cells from the SP35 cell line or 10 x 10(6) concanavalin A-stimulated syngeneic spleen cell lymphoblasts labeled with lipophilic PKH26 fluorescent dye immediately before intravenous inoculation. Labeled cells in each retina were counted at various times from 4 to 120 hours after cell transfer by fluorescence microscopic analysis of each dissociated retina. Recipient eyes were examined within the same period by light and confocal microscope. RESULTS: SP35 T cells showed a biphasic distribution in the retina. The first peak of 160 cells/retina was noted at 24 hours. A steady decline of labeled cells at 48 and 72 hours was followed by a rapid increase at 96 and 120 hours. Concanavalin A-stimulated, control-labeled cell populations showed an identical peak at 24 hours but a persistent decline thereafter; only two or three T cells were present in each retina at 120 hours. Concurrent inoculation of SP35 cells and nonspecific T cell blasts did not produce more SP35 cells than control cells in the retina at any time. Microscopic analysis showed mononuclear cell infiltration of the iris, ciliary body, and aqueous humor at 48 hours, which intensified rapidly and persisted through 120 hours. Retinal inflammation did not begin until 80 hours. Mononuclear cell adherence to vascular endothelium and perivascular macrophage infiltration of the innermost layers progressed to edema, and profound destructive inflammation and loss of retinal stratification were observed at 120 hours. CONCLUSIONS: There is no evidence of a blood-ocular or blood-retinal barrier to activated T cell blasts. Autologous S-Ag does not provoke a more rapid entry of specific T cells at that site. The data confirm that anterior segment inflammation precedes retinal inflammation, even though S-Ag-specific T cells were present in the retina within a few hours after cell transfer. Because S-Ag is clearly present in the retina, delay in antigen presentation at that site may account for the temporal difference between retinal and anterior segment inflammation.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×