Inhibition of the induction of contact hypersensitivity by an epithelial cell-derived interleukin-1 inhibitor.

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.

• Authors: L J Walsh, T W Au, G J Seymour
• Journal: The Australasian journal of dermatology (Australas J Dermatol) Vol. 30 Issue 1 Pg. 48-52 ( 1989) ISSN: 0004-8380 [Print] Australia
• PMID: 2486053 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Interleukin-1
• Interleukin-2
• Dinitrofluorobenzene

Topics

• Animals
• Cell Division
• Dermatitis, Contact (immunology)
• Dinitrofluorobenzene (immunology)
• Gingiva (cytology, immunology)
• Interleukin-1 (antagonists & inhibitors)
• Interleukin-2 (biosynthesis)
• Keratinocytes (immunology, radiation effects)
• Lymphocytes (physiology)
• Male
• Mice
• Mice, Inbred BALB C
• Spleen (cytology)