Abstract
The co-signaling molecule B7-H1 (CD274) functions as both a co-inhibitor through programmed death-1 (PD-1) receptor and a co-stimulator via an as-yet-unidentified receptor on T cells. We investigated the physiological role of endogenous B7-H1 in the pathogenesis of herpetic stromal keratitis (HSK) caused by herpes simplex virus type 1 (HSV-1). Following HSV-1 infection of the cornea of mice, B7-H1 expression was up-regulated in the CD11b+ macrophage population in the draining lymph nodes (dLN) and in the inflamed cornea. In addition, HSV-1 infection significantly increased PD-1 expression on CD4+ T cells in the dLN and inflamed cornea. The administration of antagonistic B7-H1 monoclonal antibody resulted in the proliferation of HSV-specific CD4+ T cells that secreted interferon (INF)-γ, and inhibited the apoptosis of HSV-specific CD4+ T cells, which exaggerated HSK. These results strongly suggest that the B7-H1 may be involved in suppression of the development of HSK.
Original language | English (US) |
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Pages (from-to) | 6259-6264 |
Number of pages | 6 |
Journal | FEBS Letters |
Volume | 579 |
Issue number | 27 |
DOIs | |
State | Published - Nov 7 2005 |
Keywords
- B7-H1
- Herpes simplex virus type I
- Herpetic stromal keratitis
- PD-1
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Molecular Biology