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ABSTRACT
Objectives: Along the various kinds of metal alloys used in dentistry, nickel-containing metal
alloys are extensively used for dental prostheses and orthodontic appliances. Although nickel
is known as the most common allergenic metal, the precise pathogenesis of nickel allergy has
been still unclear. In this study we analyzed the cellular and the molecular mechanism for
allergic reaction using a mouse model for nickel allergy.
Materials and Methods: Immune cells infiltrating in the inflammatory lesion in the skin from
nickel allergy model were detected by flow cytometric and immunohistochemical analysis. In
addition, regulatory T (Treg) cells purified from normal mice were transferred into nickel allergy
mice to prevent allergic immune response. The allergic lesions were investigated by
pathological and immunological analysis. Titanium was used as a control metal.
Results: CD3+ T cells (40 %) and CD19+ B cells (15 %) were infiltrated into the inflammatory
lesion of nickel allergy model. In addition, the number of Foxp3+ Treg cells and CD11c+
dendritic cells were significantly increased compared with those of control mice. Cell transfer
with Treg cell resulted in the preventive effect on nickel allergic reaction.
Conclusion: T cells including Treg cells play a key role in the pathogenesis of nickel allergy.
From our results the therapeutic strategy with Treg cell may be useful for the metal allergy.