title: Langerhans' cell count and HLA class II profile in cervical intraepithelial neoplasia in the presence or absence of HIV infection.
abstract: OBJECTIVE
  The progression of immunosuppression in human immunodeficiency virus (HIV)+ women has been correlated with elevated incidence of squamous intraepithelial lesions (SIL), probably indicating the role of local immune milieu. In this study, we analysed S100, and HLA class II molecule expression in cervical biopsies according to HIV status, to the severity of SIL and to human papillomavirus (HPV) type.
  
  
  METHODS
  Biopsies from 34 HIV+ and 44 HIV- patients with normal cervix or low- or high-grade SIL were studied. Langerhans' cells (LC) (S100), HLA class II and HLA-DQ molecules were evaluated by immunohistochemistry. HPV detection was performed using polymerase chain reaction (PCR). For statistical analysis Mann-Whitney (P< or =0.05) and Spearman test were used.
  
  
  RESULTS
  Epithelial S100 and HLA class II density were significantly increased with the severity of lesion (P=0.032; P=0.005). Epithelial S100+ increased in HPV+ (P=0.038), and HLA class II density decreased in HPV 16+ (P=0.035) or 18+ (P<0.0001) samples. HIV infection was associated with increased stromal S100+ (P=0.0005) and decreased HLA class II densities (P=0.0001). Decreased stromal S100+ was observed in women with CD4<500 cells/microl (P=0.050). Among HIV+ patients with SIL, the lowest S100 and epithelial HLA class II densities were detected in women with CD4<200 cells/microl (P=0.045).
  
  
  CONCLUSIONS
  After the establishment of AIDS, increased numbers of immature LCs and a reduction in HLA class II occurred, possibly turning the cervical milieu more favourable to HPV persistence. HPV 16 and 18 infections may interfere with the antigen presenting activity, possibly as an evasion mechanism.
authors.affiliation: Division of Clinical Immunology, Department of Medicine, School of Medicine of Ribeirão Preto, University of São Paulo, Av. Bandeirantes, 3900, 14049-900 Ribeirão Preto, São Paulo, Brazil. epigin@uol.com.br
authors.forename: M A G
authors.initials: MA
authors.lastname: Gonçalves
authors.forename: E G
authors.initials: EG
authors.lastname: Soares
authors.forename: A P M
authors.initials: AP
authors.lastname: Fernandes
authors.forename: B A L
authors.initials: BA
authors.lastname: Fonseca
authors.forename: J S R
authors.initials: JS
authors.lastname: Bettini
authors.forename: R T S
authors.initials: RT
authors.lastname: Simões
authors.forename: E A
authors.initials: EA
authors.lastname: Donadi
mesh_terms: D000328:Adult; D002452:Cell Count; D002584:Cervix Uteri / Q000473:pathology / Q000821:virology; D004279:DNA, Viral / Q000032:analysis; D005260:Female; D015658:HIV Infections / Q000276:immunology* / Q000473:pathology; D006682:HLA-DP Antigens / Q000032:analysis; D006683:HLA-DQ Antigens / Q000032:analysis; D006684:HLA-DR Antigens / Q000032:analysis; D000949:Histocompatibility Antigens Class II / Q000032:analysis*; D006801:Humans; D007150:Immunohistochemistry; D007801:Langerhans Cells / Q000473:pathology*; D008875:Middle Aged; D027383:Papillomaviridae / Q000235:genetics; D030361:Papillomavirus Infections / Q000276:immunology; D009418:S100 Proteins / Q000032:analysis; D002578:Uterine Cervical Dysplasia / Q000276:immunology* / Q000473:pathology / Q000821:virology*
chemical_list: D004279:DNA, Viral; D006682:HLA-DP Antigens; D006683:HLA-DQ Antigens; D006684:HLA-DR Antigens; D000949:Histocompatibility Antigens Class II; D009418:S100 Proteins