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Fig. 3 | Orphanet Journal of Rare Diseases

Fig. 3

From: Immunological consequences of compromised ocular immune privilege accelerate retinal degeneration in retinitis pigmentosa

Fig. 3

Blood-retinal-Barrier Study. Sodium angiography of control and rd1 indicated that the Blood retinal barrier is compromised, as seen by the extravasation dye into retina from retinal vessels (A, B). The mRNA expression profile of ocular tight junction protein displays a significant down-regulation of all proteins except ZO1 in rd1. ZO1, a RPE replication inhibiting factor is significantly up-regulated, the expressed proteins follow similar trend (C). The E cadherin was found to be significantly downregulated in rd1 (p = 0.0214) and ZO1 was overexpressed in rd1 RPE cells compared to C57BL/B6 (n = 3). The rd1 RPE layer displayed significantly higher number MHC-II expressing RPE cells which otherwise expresses only MHC-I (D). ICAM1 adhesion protein expressing RPE cells, responsible for immune cell extravasation, were also significantly increased in rd1 (E). Retinal S antigen (F) and IRBP (G) were significantly higher in rd1 peripheral circulation as compared to control. Ocular lysate was used as positive control for the retinal antigens. IRBP antigen level in serum was higher in RP patients (n = 40) compared to healthy group (n = 30) (H). Suppression of ICAM1 by neutralizing antibodies can deter monocytes. However, T-helper CD3+4+ cells can infiltrate even in the absence of ICAM1 adhesion ligand on RPE (I)

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