Document Detail


The effect of cellular immune tolerance to HSV-1 antigens on the immunopathology of HSV-1 keratitis.
MedLine Citation:
PMID:  2536358     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Previous studies have revealed that herpes simplex virus type 1 (HSV-1) corneal stromal lesions do not develop in the absence of a cell-mediated immune (CMI) response to HSV-1 antigens. HSV-1 glycoprotein C (gC) has been shown to play an important role in the induction of the cytotoxic T lymphocyte (CTL) response to HSV-1 infections at anatomical sites other than the eye. Here we report that a deletion mutant lacking gC (gC-39) when used to infect the corneas of A/J mice was a poor inducer of both CTL and delayed type hypersensitivity (DTH) responses. We have also followed histologically and immunohistochemically the course of HSV-1 stromal disease in A/J mice following topical corneal (TC) infection with wild type (WT) HSV-1, TC infection with gC-39 HSV-1, and simultaneous TC and anterior chamber (TC + AC) infection with WT HSV-1. The latter type of infection has been shown to induce a profound state of DTH and CTL tolerance of HSV-1 antigens. Following TC infection with WT HSV-1, stromal disease progressed to severe ulcerative keratitis with neovascularization by day 21. Histologic and immunohistochemical analysis revealed a predominantly mononuclear infiltrate consisting of numerous plasma cells as well as L3T4+ (T helper/inducer) and Lyt-2+ (T suppressor/cytotoxic) T lymphocytes. Following TC infection with gC-39, or simultaneous TC + AC infection with WT HSV-1, the severity of stromal disease did not progress beyond day 7. On day 21, there was at most a mild stromal cellular infiltrate consisting predominantly of polymorphonuclear neutrophils. These findings indicate that early stromal disease consists of a nonspecific inflammatory response, but severe stromal disease involves a CMI response to HSV-1. AC injection of HSV-1 inhibits the CMI response, thereby halting the progression of stromal disease. Similarly, gC-39, a poor inducer of CMI responses, is also a poor inducer of stromal disease.
Authors:
R L Hendricks; R J Epstein; T Tumpey
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Investigative ophthalmology & visual science     Volume:  30     ISSN:  0146-0404     ISO Abbreviation:  Invest. Ophthalmol. Vis. Sci.     Publication Date:  1989 Jan 
Date Detail:
Created Date:  1989-02-28     Completed Date:  1989-02-28     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  7703701     Medline TA:  Invest Ophthalmol Vis Sci     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  105-15     Citation Subset:  IM    
Affiliation:
Department of Ophthalmology, Lions of Illinois Eye Research Institute, University of Illinois College of Medicine, Chicago 60612.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, Viral / immunology*
Chromosome Deletion
Cornea / pathology
Female
Hypersensitivity, Delayed / etiology
Immune Tolerance*
Immunity, Cellular*
Immunohistochemistry
Keratitis, Dendritic / complications,  immunology*,  pathology
Mice
Mice, Inbred Strains
Simplexvirus / genetics,  immunology*
T-Lymphocytes, Cytotoxic / physiology
Viral Envelope Proteins / genetics
Grant Support
ID/Acronym/Agency:
EY 01792/EY/NEI NIH HHS; EY 05945/EY/NEI NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, Viral; 0/Viral Envelope Proteins; 0/glycoprotein gC, herpes simplex virus type 1

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