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(Investigative Ophthalmology and Visual Science. 2006;47:3400-3409.)
© 2006 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.05-0898
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CD8 T Cells Mediate Transient Herpes Stromal Keratitis in CD4-Deficient Mice

Andrew J. Lepisto,1 Gregory M. Frank,2,3 Min Xu,4 Patrick M. Stuart,5,6 and Robert L. Hendricks1,2,7

1From the Departments of Immunology, 2Ophthalmology, and 7Molecular Genetics and Biochemistry, and the 3Graduate Program in Immunology, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania; the 4Department of Surgery, University of Pennsylvania, Philadelphia, Pennsylvania; and the 5Departments of Ophthalmology and Visual Sciences and 6Molecular Microbiology and Pathogenesis, Washington University School of Medicine, St. Louis, Missouri.

PURPOSE. To evaluate the role of CD4+ T cells in the development of murine herpes stromal keratitis (HSK).

METHODS. The corneas of wild-type (WT) BALB/c mice and three types of CD4-deficient BALB/c mice (CD4–/–, CD4-depleted, CD4 and CD8 double-depleted) were infected with different doses of HSV-1 RE, and HSK incidence and severity were monitored. Corneal infiltrates were quantitatively and functionally assayed by flow cytometric analysis of individually digested diseased corneas and documented histologically.

RESULTS. At a relatively high infectious dose (1 x 105 pfu/cornea): (1) CD4-deficient and WT BALB/c mice had severe HSK with a similar incidence (80%–100%), whereas HSK did not develop in mice deficient in both CD4+ and CD8+ T cells; (2) neutrophils were the predominate leukocyte in the corneas of CD4-deficient and WT mice; (3) the corneas of WT mice had activated, HSV-1-specific CD4+ T cells, but few if any CD8+ T cells; (4) the corneas of CD4-deficient mice had activated, HSV-1-specific CD8+ T cells; and (5) HSK in CD4-deficient mice was transient, showing loss of CD8+ T cells at 2 to 3 weeks after infection (pi) followed by a loss of neutrophils. At a relatively low infectious dose of HSV-1 (103 pfu/cornea) severe HSK developed in 80% to 90% of WT mice, but in only 30% to 40% of CD4-deficient mice.

CONCLUSIONS. CD4+ T cells preferentially mediate HSK, but, in their absence, a high infectious dose of HSV-1 can induce histologically similar but transient HSK that is mediated by CD8+ T cells.




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