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Elucidating the protective and pathologic T cell species in the virus‐induced corneal immunoinflammatory condition herpetic stromal keratitis
Author(s) -
Banerjee Kaustuv,
Biswas Partha Sarathi,
Rouse Barry T.
Publication year - 2005
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0904486
Subject(s) - biology , t cell , cd8 , stromal cell , adoptive cell transfer , immune system , immunology , population , herpes simplex virus , cytotoxic t cell , pathogenesis , virology , epitope , virus , antibody , cancer research , in vitro , medicine , genetics , environmental health
Herpetic stromal keratitis (HSK) results in postinfection with Herpes simplex virus type 1 (HSV‐1). The pathogenesis involves tissue damage by the host immune system, classifying HSK as an immunopathological disease. The crucial disease orchestrating cells is thought to be the T lymphocytes. The present study elucidates pathogenic and protective T cell subsets involved in the development of HSK using the gBT mice, which possess a monoclonal population of CD8 + T cells reactive to a HSV immunodominant epitope. Results show that HSV‐reactive CD8 + T cells enter infected corneas during the acute but not the chronic phase of the disease during which the predominant population is CD4 + T cells. Adoptive transfer experiments in T and B cell‐deficient recombination‐activating gene knockout mice revealed that HSV‐reactive CD8 + T cells are capable of ocular virs clearance, possibly through a combination of corneal and peripheral nervous system antiviral effects, but are not involved in lesion development. CD4 + T cells of the virus‐specific or nonspecific species emerged as the pathogenic T cells capable of precipitating disease. These observations have the potential to yield important treatment strategies by targeting specific cell types in HSK.