Abstract
Interleukin-1 (IL-1) is the central hormone of acute inflammation. Previous studies have demonstrated that an Interleukin-1 inhibitor (ILS) derived from human gingival epithelial cell cultures abrogates the effect of IL-1 on human Langerhans cells and murine thymocytes in vitro. The present study investigated the effect of ILS on the induction and elicitation of contact hypersensitivity (CHS) to 2,4-dinitro-1-fluorobenzene (DNFB). Systemic administration of ILS 6 days prior to sensitisation significantly blocked the induction of CHS to DNFB in Balb/c mice. In addition, i.v. injection of ILS 24 or 48 hours prior to the elicitation of CHS produced a reduction in ear swelling, but the suppressive effect was less profound than when ILS was administered prior to sensitisation. Thus, ILS production by epithelial cells is a possible mechanism for the down-regulation of cutaneous immune responses.
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