June 1988
Volume 29, Issue 6
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Articles  |   June 1988
Modulation of HLA antigen expression on corneal epithelial and stromal cells.
Author Affiliations
  • N G Dreizen
    Department of Ophthalmology, Georgetown University Medical Center, Washington, DC 20007.
  • C F Whitsett
    Department of Ophthalmology, Georgetown University Medical Center, Washington, DC 20007.
  • R D Stulting
    Department of Ophthalmology, Georgetown University Medical Center, Washington, DC 20007.
Investigative Ophthalmology & Visual Science June 1988, Vol.29, 933-939. doi:
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      N G Dreizen, C F Whitsett, R D Stulting; Modulation of HLA antigen expression on corneal epithelial and stromal cells.. Invest. Ophthalmol. Vis. Sci. 1988;29(6):933-939.

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Abstract

Human corneal epithelial cells and stromal fibroblasts in culture were incubated with gamma interferon or with medium conditioned by phytohemagglutinin (PHA)-stimulated mononuclear cells. The corneal cells were placed into suspension, assayed for class I (HLA-A,B,C) and class II (HLA-DR) antigens by indirect immunofluorescence, and analyzed with flow cytometry. Epithelial cells treated for 5 days with conditioned medium (CND-M) did not exhibit an increase in class I or an induction of class II antigen expression, although a trend toward increased class I antigen expression was present. Epithelial cells treated for 5 days with 250-500 U/ml of gamma interferon did not demonstrate an increase in class I but did show an induction of class II antigen expression; again, however, a trend toward increased class I antigen expression was present. Stromal fibroblasts treated for 3-5 days with CND-M exhibited an increase in class I antigen expression, but stromal fibroblasts treated for 1-5 days with CND-M did not show an induction of class II antigen expression. Stromal fibroblasts incubated for 1-5 days with 250-750 U/ml of gamma interferon demonstrated both an increase in class I and an induction of class II antigen expression. These data suggest that host lymphokines may intensify the process of corneal graft rejection by augmenting class I antigen expression on allogeneic cells. Moreover, the induction of class II antigen expression by host lymphokines on cells in transplanted corneal tissue may lead to host sensitization and subsequent allograft rejection.

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