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

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. (J Allergy Clin Immunol 1998;102:645-50.)