B7-H1 (CD274) inhibits the development of herpetic stromal keratitis (HSK)

Her Jun, Su K. Seo, Hye Young Jeong, Hyoun Mi Seo, Gefeng Zhu, Lieping Chen, In Hak Choi

Research output: Contribution to journalArticlepeer-review

29 Scopus citations


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 languageEnglish (US)
Pages (from-to)6259-6264
Number of pages6
JournalFEBS Letters
Issue number27
StatePublished - Nov 7 2005


  • B7-H1
  • Herpes simplex virus type I
  • Herpetic stromal keratitis
  • PD-1

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology


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