INFLUENCE OF VIRAL-INFECTION ON EXPRESSION OF CELL-SURFACE ANTIGENS IN HUMAN RETINAL-PIGMENT EPITHELIAL-CELLS

Citation
C. Larcher et al., INFLUENCE OF VIRAL-INFECTION ON EXPRESSION OF CELL-SURFACE ANTIGENS IN HUMAN RETINAL-PIGMENT EPITHELIAL-CELLS, Graefe's archive for clinical and experimental ophthalmology, 235(11), 1997, pp. 709-716
Citations number
36
Categorie Soggetti
Ophthalmology
ISSN journal
0721832X
Volume
235
Issue
11
Year of publication
1997
Pages
709 - 716
Database
ISI
SICI code
0721-832X(1997)235:11<709:IOVOEO>2.0.ZU;2-Y
Abstract
Background: Subacute viral infection is known to change the phenotype of infected cells, thereby causing immune-mediated tissue damage. The aim of this study was to investigate the expression of different cell surface molecules on human retinal pigment epithelial cells (RPEC) fol lowing viral infection, with special emphasis on those having immunore gulatory functions. Methods: Cultured RPEC were infected with cytomega lovirus (CMV), coxsackievirus B3 (CVB) or herpes simplex virus type I( HSV). Double-staining fluorescence technique was used for visualizatio n of virus infection and cell surface markers in the same cells by las er microscopy. Results: CMV downregulated MHC class I antigens on RPEC , whereas CVB and HSV did not alter MHC class I antigen expression. No induction of class II antigens was observed in RPEC infected with CVB , HSV or CMV. The intercellular adhesion molecule ICAM-1 (CD54) was st rongly expressed in uninfected RPEC, and a slight increase was observe d after virus infection. Vascular cell adhesion molecule 1 (VCAM-1) wa s expressed in low amounts in both uninfected and infected RPEC. No ex pression of intercellular adhesion molecule 2 (ICAM-2), E-selectin ELA M-1 or lymphocyte-function-associated antigen 1 (LFA-1) was observed o n RPEC before or after virus infection. Conclusion: Downmodulation of immune-regulating cell surface antigens has been suggested to provide a means of long-term survival of viruses in the infected cell, favorin g establishment of persistent infection. Our observation in cultured h uman RPEC indicates that this mechanism might indeed contribute to the development of disease affecting retinal tissue.