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(American Journal of Pathology. 2000;156:1139-1149.)
© 2000 American Society for Investigative Pathology


Short Communications

Breakdown of the Blood-Retinal Barrier Induced by Activated T Cells of Nonneural Specificity

Ping Hu*, John D. Pollard{dagger} and Tailoi Chan-Ling*

From the Department of Anatomy and Histology and Institute of Biomedical Research*
and the Department of Medicine,{dagger}
University of Sydney, Sydney, New South Wales, Australia

The cellular and microvascular responses of JC Lewis rats to an intravenous injection of activated T cells specific for ovalbumin were examined with the retinal whole mount technique. The retina was examined at various times post-injection (pi) with the use of antibodies to the {alpha}ß T cell receptor (TCR) or to major histocompatibility complex class II (MHC II), the monoclonal antibody ED1, and intravascular tracers. By 12 hours pi, small numbers of TCR+, ED1+, and MHC II+ cells were present within the lumen of retinal vessels, and minor breakdown of the blood-retinal barrier (BRB) and microglial activation were evident. The intensity of these responses had increased by 1 day pi, when small numbers of TCR+ cells had also undergone extravasation. By 2 to 3 days pi, the numbers of TCR+, ED1+, and MHC II+ cells in the retinal parenchyma had increased, but the BRB breakdown and microglial activation had subsided. Thus, in the absence of target antigen, activated T cells induced limited and transient breakdown of the BRB, microglial activation, and the extravasation of ED1+, MHC II+ monocytes. In contrast, the retina of rats that received an intraocular injection of ovalbumin in addition to the intravascular injection of T cells showed massive cellular recruitment and breakdown of the BRB. These results indicate that an increase in the number of activated T cells in the circulation, such as that which occurs during viral or bacterial infection, has the potential to result in transient breakdown of the BRB and a mild local microglial response.





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