December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Role of CD4 and CD8 T Cell Subsets in a Murine Model of Primary HSK
Author Affiliations & Notes
  • PM Stuart
    Ophthalmology & Visual Science and Molecular Microbiology & Pathogenesis Washington University Eye Center St Louis MO
  • B Summers
    Ophthalmology & Visual Science and Molecular Microbiology & Pathogenesis
    Washington University Eye Center St Louis MO
  • JE Morris
    Ophthalmology & Visual Sciences
    Washington University Eye Center St Louis MO
  • TL Keadle
    Ophthalmology & Visual Sciences
    Washington University Eye Center St Louis MO
  • DA Leib
    Ophthalmology & Visual Science and Molecular Microbiology & Pathogenesis
    Washington University Eye Center St Louis MO
  • Footnotes
    Commercial Relationships   P.M. Stuart, None; B. Summers, None; J.E. Morris, None; T.L. Keadle, None; D.A. Leib, None. Grant Identification: NIH Grant EY11885
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 30. doi:
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    • Get Citation

      PM Stuart, B Summers, JE Morris, TL Keadle, DA Leib; Role of CD4 and CD8 T Cell Subsets in a Murine Model of Primary HSK . Invest. Ophthalmol. Vis. Sci. 2002;43(13):30.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose:To better define the role that specific T cell subsets play during primary herpetic stromal keratitis (HSK). Methods:We infected the corneas of BALB/c, BALB-CD4 KO, BALB-CD8 KO and anti-CD8 treated BALB/c and anti-CD4 treated BALB/c with HSV-1, KOS strain virus. We also infected the corneas of C57BL/6 (B6), B6-CD4 KO, and B6-CD8 KO mice with HSV-1, McKrae strain virus. These mice were then evaluated for HSK disease, spread of viral infection, and viral load in the trigeminal ganglia. Results:Mice that lack CD8+ T cells demonstrated significantly more disease than did either BALB/c or B6 parental strains. In contrast mice without CD4+ T cells had less disease than parental controls. Infectious virus persisted slightly longer in the cornea, trigeminal ganglia, and periocular tissue in mice without CD4 or CD8 T cells. There were no significant differences in viral genome copies in trigeminal ganglia with latent viral infection. Interestingly, the incidence of viral encephalitis was greatest in mice without CD8 T cells, and virtually non-existent in mice without CD4 T cells. Conclusion:These data support the thesis that CD4+ T cells are not required for resistence to infection with HSV-1. However, they likely are the primary mediators for the development of HSK. They also suggest that CD8+ T cells play a protective role, either in controlling the viral disease, or in regulating the inflammatory immune response that mediates HSK.

Keywords: 425 herpes simplex virus • 469 microbial pathogenesis: experimental studies • 449 keratitis 
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