title: Pityriasis lichenoides et varioliformis acuta and pityriasis lichenoides chronica: comparison of lesional T-cell subsets and investigation of viral associations.
abstract: BACKGROUND
  Pityriasis lichenoides (PL) exhibits a broad clinical spectrum that includes both acute and chronic forms. The precise biologic mechanisms underlying PL remain unclear.
  
  
  OBJECTIVE
  To evaluate the immunohistochemical characteristics of PL and to investigate lesional T-cell subsets and the possible role of viral infection in its pathogenesis.
  
  
  METHODS
  Samples from 10 patients with PL et varioliformis acuta (PLEVA) and 13 with PL chronica (PLC) were analyzed immunohistochemically. Epstein-Barr virus early regions were assayed by in situ hybridization and T-cell receptor-γ (TCR-γ) gene rearrangements were assayed by polymerase chain reaction (PCR). We also utilized PCR to assay for human herpesvirus-8 (HHV-8) DNA in 51 patients with PL and in 25 controls.
  
  
  RESULTS
  Lymphocytes expressing CD8 and T-cell intracellular antigen-1 were more abundant in patients with PLEVA than with PLC, whereas CD4+ lymphocytes and FOXP3-positive regulatory T-cells were more abundant in PLC. HHV-8 DNA was present in 11 of 51 (21.6%) PL patients and 0 of 25 controls. A clonal TCR-γ gene rearrangement was observed in only one patient with PLEVA.
  
  
  CONCLUSIONS
  Our data suggests that PL may represent an inflammatory condition induced by various triggering agents, such as HHV-8, rather than a lymphoproliferative disorder. PLEVA, characterized by an acute course with severe symptoms, may indicate a relative lack of regulatory T-cells in comparison with PLC.
authors.affiliation: Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
authors.forename: Jeong Eun
authors.initials: JE
authors.lastname: Kim
authors.forename: Woo Jin
authors.initials: WJ
authors.lastname: Yun
authors.forename: Seog-Kyun
authors.initials: SK
authors.lastname: Mun
authors.forename: Ghil Suk
authors.initials: GS
authors.lastname: Yoon
authors.forename: Jooryung
authors.initials: J
authors.lastname: Huh
authors.forename: Jee Ho
authors.initials: JH
authors.lastname: Choi
authors.forename: Sungeun
authors.initials: S
authors.lastname: Chang
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000368:Aged; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism / Q000473:pathology; D002648:Child; D002675:Child, Preschool; D002908:Chronic Disease; D004279:DNA, Viral / Q000032:analysis; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000378:metabolism; D004854:Herpesvirus 4, Human / Q000235:genetics / Q000302:isolation & purification; D019288:Herpesvirus 8, Human / Q000235:genetics / Q000302:isolation & purification; D006801:Humans; D017403:In Situ Hybridization; D008297:Male; D008875:Middle Aged; D017514:Pityriasis Lichenoides / Q000378:metabolism / Q000473:pathology* / Q000821:virology; D016133:Polymerase Chain Reaction; D012867:Skin / Q000378:metabolism / Q000473:pathology / Q000821:virology; D016176:T-Lymphocyte Subsets / Q000378:metabolism / Q000473:pathology* / Q000821:virology; D050378:T-Lymphocytes, Regulatory / Q000473:pathology; D055815:Young Adult
chemical_list: D004279:DNA, Viral; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors