title: Association of increased CD4+ T-cell infiltration with increased IL-16 gene expression in atopic dermatitis.
abstract: BACKGROUND
  The mechanisms involved in the initiation and the maintenance of skin inflammation in atopic dermatitis (AD) are poorly understood. Previous studies have demonstrated increased numbers of infiltrating CD4+ T cells in acute lesions compared with normal control skin. IL-16 is a cytokine that has selective chemotactic activity for CD4+ cells.
  
  
  OBJECTIVE
  We sought to examine whether IL-16 expression might be upregulated in acute versus chronic AD.
  
  
  METHODS
  We investigated the expression of IL-16 mRNA in skin biopsy specimens from acute and chronic skin lesions, as well as from the uninvolved skin of patients with AD and normal skin. Cryostat sections from 4% paraformaldehyde-fixed skin biopsy specimens were processed for in situ hybridization by using cRNA coding for IL-16 mRNA. Numbers of infiltrating CD4+ and CD8+ cells were also determined by immunocytochemistry.
  
  
  RESULTS
  There were positive signals for IL-16 mRNA both in the basal layer of the epidermis and in the dermis of AD skin biopsy specimens from all subjects studied. The numbers of epidermal and dermal IL-16 mRNA+ cells were significantly increased in acute skin lesions compared with chronic (P <.01) and uninvolved (P <.001) skin lesions and compared with normal skin (P <.001). The number of CD4+ cells was significantly increased in acute skin lesions compared with chronic (P <.01) skin lesions and uninvolved skin (P <.01) and compared with normal skin (P <.01). Significant correlations were found between the numbers of CD4+ cells and the numbers of epidermal (r = 0.82, P <.001) and dermal (r = 0.71, P <.001) IL-16 mRNA+ cells.
  
  
  CONCLUSIONS
  The results demonstrate that upregulation of IL-16 mRNA expression in acute AD is associated with increased numbers of CD4+ cells, suggesting that IL-16 may play a role in the initiation of skin inflammation, presumably through recruitment of CD4+ cells.
authors.affiliation: Meakins-Christie Laboratories, Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.
authors.forename: S
authors.initials: S
authors.lastname: Laberge
authors.forename: O
authors.initials: O
authors.lastname: Ghaffar
authors.forename: M
authors.initials: M
authors.lastname: Boguniewicz
authors.forename: D M
authors.initials: DM
authors.lastname: Center
authors.forename: D Y
authors.initials: DY
authors.lastname: Leung
authors.forename: Q
authors.initials: Q
authors.lastname: Hamid
mesh_terms: D001706:Biopsy; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D003876:Dermatitis, Atopic / Q000235:genetics* / Q000276:immunology*; D015870:Gene Expression; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D019410:Interleukin-16 / Q000235:genetics*; D012333:RNA, Messenger / Q000378:metabolism; D012867:Skin / Q000276:immunology / Q000473:pathology
chemical_list: D019410:Interleukin-16; D012333:RNA, Messenger