Breakdown of the blood-retinal barrier induced by activated T cells of nonneural specificity

The cellular and microvascular responses of JC Lewis rats to an intravenous injection of activated T cells specific for ovalbumin were examined with t he retinal whole mount technique. The retina was examined at various times post-injection (pi) with the use of antibodies to the alpha beta T cell rec eptor (TCR) or to major histocompatibility complex class IT (MHC II), the m onoclonal antibody ED1, and intravascular tracers. By 12 hours pi, small nu mbers of TCR+, ED1(+), and MHC II+ cells were present within the lumen of r etinal vessels, and minor breakdown of the blood-retinal barrier (BRB) and microglial activation were evident. The intensity of these responses had in creased by I day pi, when small numbers of TCR+ cells had also undergone ex travasation, By 2 to 5 days pi, the numbers of TCR+, ED1(+), and MHC II+ ce lls in the retinal parenchyma had increased, but the BRB breakdown and micr oglial activation had subsided. Thus, in the absence of target antigen, act ivated T cells induced limited and transient breakdown of the BRB, microgli al activation, and the extravasation of ED1(+), MHC II+ monocytes, In contr ast, the retina of rats that received an intraocular injection of ovalbumin in addition to the intravascular injection of T tells showed massive cellu lar recruitment and breakdown of the BRB, These results indicate that an in crease in the number of activated T cells in the circulation, such as that which occurs during viral or bacterial infection, has the potential to resu lt in transient breakdown of the BRB and a mild local. microglial response.