3.8 Article

Lack of evidence for local immune activity in oral hairy leukoplakia and oral wart lesions

Journal

ORAL MICROBIOLOGY AND IMMUNOLOGY
Volume 20, Issue 3, Pages 154-162

Publisher

WILEY
DOI: 10.1111/j.1399-302X.2005.00198.x

Keywords

cytokines; HIV; oral hairy leukoplakia; oral warts; T cells

Funding

  1. NIDCR NIH HHS [DE 12178] Funding Source: Medline

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Background: Oral warts, caused by human papillomavirus (HPV), and oral hairy leukoplakia (OHL) caused by Epstein-Barr virus (EBV), are common oral manifestations in HIV-infected persons. Although both conditions occur most often with reduced blood CD4(+) T-cell numbers, oral warts and OHL rarely occur simultaneously, suggesting that dysfunctions in other secondary local immune parameters are also involved. The present study evaluated tissue-associated proinflammatory and T-helper cytokine and chemokine mRNA expression and the presence of T cells in each lesion. Methods: Biopsies were taken from lesion-positive and adjacent lesion-negative sites of HIV+ persons with oral warts or OHL and lesion-negative sites from HIV+ persons who were oral HPV or EBV DNA-positive (matched controls). Cytokine/chemokine mRNA expression was quantified by real-time polymerase chain reaction. CD3, CD4, and CD8 cells were identified by immunohistochemistry. Results: No differences were detected in tissue-associated cytokine/chemokine mRNA expression in warts or OHL when compared to lesion-negative sites. Immunohistochemical analysis of T cells showed CD8(+) cells exclusively, but few cells were present in either lesion. No differences were detected between lesion-positive and -negative control sites of each pathologic condition. Conclusion: Little evidence was found for local immune reactivity to either oral warts and OHL, suggesting that CD4(+) T cells are a primary host defense against both oral warts and OHL, but with nonimmune factors potentially responsible for the divergent prevalence of each.

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