Inhibition of the induction of contact hypersensitivity by an epithelial cell-derived interleukin-1 inhibitor.
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.
Walsh
L J
LJ
Au
T W
TW
Seymour
G J
GJ
D000818:Animals; D002455:Cell Division; D003877:Dermatitis, Contact / Q000276:immunology*; D004139:Dinitrofluorobenzene / Q000276:immunology; D005881:Gingiva / Q000166:cytology / Q000276:immunology; D007375:Interleukin-1 / Q000037:antagonists & inhibitors*; D007376:Interleukin-2 / Q000096:biosynthesis; D015603:Keratinocytes / Q000276:immunology* / Q000528:radiation effects; D008214:Lymphocytes / Q000502:physiology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D013154:Spleen / Q000166:cytology
D007375:Interleukin-1; D007376:Interleukin-2; D004139:Dinitrofluorobenzene