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INHIBITION OF THE INDUCTION OF CONTACT HYPERSENSITIVITY BY AN EPITHELIAL CELL‐DERIVED INTERLEUKIN‐1 INHIBITOR
Author(s) -
Walsh Laurence J.,
Au Tony W.,
Seymour Gregory J.
Publication year - 1989
Publication title -
australasian journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.67
H-Index - 53
eISSN - 1440-0960
pISSN - 0004-8380
DOI - 10.1111/j.1440-0960.1989.tb00410.x
Subject(s) - medicine , interleukin , delayed hypersensitivity , immune system , inflammation , immunology , in vitro , pharmacology , cytokine , biology , biochemistry
S ummary 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.