February 1990
Volume 31, Issue 2
Free
Articles  |   February 1990
Histology and immunohistology of Igh-1-restricted herpes simplex keratitis in BALB/c congenic mice.
Author Affiliations
  • E M Opremcak
    Department of Ophthalmology, Ohio State University College of Medicine, Columbus 43210.
  • B A Rice
    Department of Ophthalmology, Ohio State University College of Medicine, Columbus 43210.
  • P A Wells
    Department of Ophthalmology, Ohio State University College of Medicine, Columbus 43210.
  • C S Foster
    Department of Ophthalmology, Ohio State University College of Medicine, Columbus 43210.
Investigative Ophthalmology & Visual Science February 1990, Vol.31, 305-312. doi:
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      E M Opremcak, B A Rice, P A Wells, C S Foster; Histology and immunohistology of Igh-1-restricted herpes simplex keratitis in BALB/c congenic mice.. Invest. Ophthalmol. Vis. Sci. 1990;31(2):305-312.

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Abstract

In order to characterize the local ocular immunologic milieu of Igh-1-restricted herpes simplex keratitis (HSK), we investigated histologic and immunohistologic correlates of disease over a 21-day time course. Clinically observable keratitis began 10 days postinoculation in susceptible C.AL-20 (Igh-1d) and moderately susceptible BALB/c (Igh-1a) mice, whereas HSV-1-resistant C.B-17 (Igh-1b) mice rarely developed disease. Igh-1-restricted histologic differences were observed by day 11 postinoculation; C.AL-20 and BALB/c mice showed augmented recruitment of neutrophils and mononuclear cells in conjunctival, limbal, and corneal tissues compared to C.B-17 mice. On immunohistologic study, Lyt-1 to Lyt-2 cell ratios by day 11 postinoculation were 7:1, 2:1, and 1:8 in corneas from C.AL-20, BALB/c, and C.B-17 mice, respectively. Macrophages and neutrophils were absent in corneas from C.B-17 mice at this time, but could be found in large numbers in the corneas of susceptible mouse strains through day 21. These data demonstrate a strong relationship between Igh-1 phenotype and inflammatory cell recruitment in response to corneal infection with HSV-1, and support a role for T cell subpopulations in mediating Igh-1-restricted HSK.

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