title: Lack of evidence for local immune activity in oral hairy leukoplakia and oral wart lesions.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Microbiology, Immunology, and Parasitology, Section of Infectious Disease, Lousiana State University Health Sciences Center and School of Dentistry, New Orleans, LA 70119, USA.
authors.forename: E A
authors.initials: EA
authors.lastname: Lilly
authors.forename: J E
authors.initials: JE
authors.lastname: Cameron
authors.forename: K V
authors.initials: KV
authors.lastname: Shetty
authors.forename: J E
authors.initials: JE
authors.lastname: Leigh
authors.forename: S
authors.initials: S
authors.lastname: Hager
authors.forename: K M
authors.initials: KM
authors.lastname: McNulty
authors.forename: C
authors.initials: C
authors.lastname: Cheeks
authors.forename: M E
authors.initials: ME
authors.lastname: Hagensee
authors.forename: P L
authors.initials: PL
authors.lastname: Fidel
mesh_terms: D017088:AIDS-Related Opportunistic Infections / Q000276:immunology* / Q000821:virology; D017252:CD3 Complex / Q000032:analysis; D015704:CD4 Antigens / Q000032:analysis; D016827:CD8 Antigens / Q000032:analysis; D018925:Chemokines / Q000032:analysis; D016207:Cytokines / Q000032:analysis; D004854:Herpesvirus 4, Human / Q000235:genetics; D006801:Humans; D007150:Immunohistochemistry; D017733:Leukoplakia, Hairy / Q000276:immunology* / Q000821:virology; D027383:Papillomaviridae / Q000235:genetics; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000302:isolation & purification; D018709:Statistics, Nonparametric; D014860:Warts / Q000276:immunology* / Q000821:virology
chemical_list: D017252:CD3 Complex; D015704:CD4 Antigens; D016827:CD8 Antigens; D018925:Chemokines; D016207:Cytokines; D012333:RNA, Messenger