title: Immunophenotype of skin lymphocytic infiltrate in patients co-infected with Mycobacterium leprae and human immunodeficiency virus: a scenario dependent on CD8+ and/or CD20+ cells.
abstract: BACKGROUND
  Leprosy occurs rarely in human immunodeficiency virus (HIV)-positive patients. In contrast to tuberculosis, there has been no report to date of an increase in HIV prevalence among patients with leprosy or of differences in leprosy's clinical spectrum. While several studies describe the systemic immune response profile in patients co-infected with HIV and leprosy, the local immune skin response has been evaluated in only a small number of case reports and limited series of patients.
  
  
  OBJECTIVE
  To investigate the interaction between Mycobacterium leprae and HIV infection in the skin.
  
  
  METHODS
  We investigated the presence and frequency of cells positive for CD4, CD8, CD20, TIA-1, FOXP3 and CD123 in lymphocytic infiltrates from 16 skin biopsies taken from 15 patients with HIV-leprosy co-infection.
  
  
  RESULTS
  CD4+ cells were absent in infiltrates from 6 (38%) skin biopsies and present in 10 (62%) cases at low levels (<1·16%) of the lymphocytic infiltrate. CD8+ was the predominant phenotype in the infiltrate (99·4%), followed by TIA-1, expressed by >75% of CD8+ cells. FOXP3+ cells were also present, representing 3·4% of the lymphocytic infiltrate. CD20+ cells were detected in 75% of the cases; however, in two cases (12%) these cells represented 25-50% of the infiltrate, while in the other 10 cases (62%) they were present only focally (<25% of the infiltrate). CD123+ cells were not observed in any of the studied specimens.
  
  
  CONCLUSIONS
  Data presented here suggest that cell-mediated immune responses to M. leprae are preserved at the site of disease and that in the absence of CD4+ cells, CD8+FOXP3+ and CD20+ cells may be involved in granuloma formation.
authors.affiliation: Department of Dermatology, Medical University of Graz, Graz, Austria.
authors.forename: C
authors.initials: C
authors.lastname: Massone
authors.forename: C
authors.initials: C
authors.lastname: Talhari
authors.forename: S
authors.initials: S
authors.lastname: Talhari
authors.forename: A M G
authors.initials: AM
authors.lastname: Brunasso
authors.forename: T M
authors.initials: TM
authors.lastname: Campbell
authors.forename: P
authors.initials: P
authors.lastname: Curcic
authors.forename: L
authors.initials: L
authors.lastname: Cerroni
authors.forename: R
authors.initials: R
authors.lastname: Ribeiro-Rodrigues
mesh_terms: D000328:Adult; D018951:Antigens, CD20 / Q000276:immunology*; D001706:Biopsy; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D016022:Case-Control Studies; D005260:Female; D051858:Forkhead Transcription Factors / Q000378:metabolism; D006099:Granuloma / Q000276:immunology; D015658:HIV Infections / Q000150:complications / Q000276:immunology* / Q000473:pathology; D006801:Humans; D016130:Immunophenotyping; D053650:Interleukin-3 Receptor alpha Subunit / Q000378:metabolism; D007918:Leprosy / Q000150:complications / Q000276:immunology* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009166:Mycobacterium leprae / Q000276:immunology; D039102:Poly(A)-Binding Proteins / Q000378:metabolism; D012867:Skin / Q000276:immunology / Q000473:pathology; D012874:Skin Diseases, Infectious / Q000276:immunology* / Q000473:pathology; D000074019:T-Cell Intracellular Antigen-1; D055815:Young Adult
chemical_list: D018951:Antigens, CD20; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; C115022:IL3RA protein, human; D053650:Interleukin-3 Receptor alpha Subunit; D039102:Poly(A)-Binding Proteins; D000074019:T-Cell Intracellular Antigen-1; C071558:TIA1 protein, human