Journal
JOURNAL OF IMMUNOLOGY
Volume 172, Issue 7, Pages 4123-4132Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.172.7.4123
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- NEI NIH HHS [EY-050093] Funding Source: Medline
- NIAID NIH HHS [AI-14981] Funding Source: Medline
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CD4(+)CD25(+) regulatory T cells (T-reg) can inhibit a variety of autoimmune and inflammatory diseases, but their involvement in regulating virus-induced immunopathology is not known. We have evaluated the role of T-reg in viral immunopathological lesion stromal keratitis. This frequent cause of human blindness results from a T cell-mediated immunoinflammatory response to HSV in the corneal stroma. The results show that lesions were significantly more severe if mice were depleted of T-reg before infection. The T-reg was also shown to modulate lesion expression induced by adoptive transfer of pathogenic CD4(+) T cells in infected SCID recipients. The mechanism of T-reg control of stromal keratitis involved suppressed antiviral immunity and impaired expression of the molecule required for T cell migration to lesion sites. Interestingly, T-reg isolated from ocular lesions in nondepleted mice showed in vitro inhibitory effects involving IL-10, but were not very effective in established lesions. Our results decipher the in vivo role of T-reg, in a virus-induced immunopathology and imply that manipulation of regulatory cell function represents a useful approach to control viral-induced immunoinflammatory disease.
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