title: The effect of VAS972 on allergic contact hypersensitivity.
abstract: BACKGROUND
  Contact hypersensitivity (CHS) is a Th1-mediated immune response that can be down-regulated by immunosuppressive agents such as cyclosporine and environmental stimuli such as ultraviolet light. Recently, an immunomodulation therapy, VAS972, has been developed which is believed to down-regulate the Th1 arm of the immune response. This VAS972 involves modifying autologous blood by controlled exposure to the oxidizing agent ozone and UVC light, at an elevated temperature ex vivo. The processed blood is then administered by intramuscular injection.
  
  
  OBJECTIVE
  To further evaluate the immune modulating effect of VAS972.
  
  
  METHODS
  We examined the effect of VAS972 treatment on CHS. Contact hypersensitivity was induced with dinitrofluorobenzene (DNFB) in animals receiving VAS972- processed blood, control blood, or saline. A preliminary study was also conducted to evaluate the effect of plasma and cellular fractions of processed blood.
  
  
  RESULTS
  Mice injected with VAS972-processed blood demonstrated a significantly lower (46%) CHS response than controls. Histologic examination of challenged ear skin from control mice displayed edema with a significant lymphocytic infiltration, whereas animals administered processed blood demonstrated a reduction in lymphocytic infiltration. Mice injected with either plasma or the cellular fraction of the VAS972-treated blood also demonstrated a significant suppression (49% and 41%, respectively).
  
  
  CONCLUSIONS
  The results of this study demonstrated that VAS972 suppresses CHS and cellular infiltration. Furthermore, the plasma and cellular components of the VAS972 treatment were also able to induce immunosuppression. This further supports the hypothesis that VAS972 down-regulates the Th1 arm of the immune response.
authors.affiliation: Division of Dermatology, Sunnybrook and Women's College Health Science Centre, University of Toronto, Toronto, Ontario, Canada.
authors.forename: G M
authors.initials: GM
authors.lastname: Shivji
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
authors.forename: A S
authors.initials: AS
authors.lastname: Mandel
authors.forename: A E
authors.initials: AE
authors.lastname: Bolton
authors.forename: D N
authors.initials: DN
authors.lastname: Sauder
mesh_terms: D000818:Animals; D016913:Blood Component Transfusion; D001804:Blood Transfusion, Autologous; D017449:Dermatitis, Allergic Contact / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D004139:Dinitrofluorobenzene / Q000633:toxicity; D007273:Injections, Intramuscular; D051379:Mice; D008807:Mice, Inbred BALB C; D012867:Skin / Q000187:drug effects / Q000473:pathology; D018417:Th1 Cells / Q000187:drug effects / Q000276:immunology
chemical_list: D004139:Dinitrofluorobenzene