Association of increased CD4+ T-cell infiltration with increased IL-16 gene expression in atopic dermatitis

J Allergy Clin Immunol. 1998 Oct;102(4 Pt 1):645-50. doi: 10.1016/s0091-6749(98)70282-9.


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.

Conclusion: 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biopsy
  • CD4-Positive T-Lymphocytes / immunology*
  • Dermatitis, Atopic / genetics*
  • Dermatitis, Atopic / immunology*
  • Gene Expression*
  • Humans
  • Immunohistochemistry
  • In Situ Hybridization
  • Interleukin-16 / genetics*
  • RNA, Messenger / metabolism
  • Skin / immunology
  • Skin / pathology


  • Interleukin-16
  • RNA, Messenger