Background: Allergic contact dermatitis (ACD) resulting from exposure to low molecular weight chemicals is a common clinical condition in industrialized countries and can be mediated by either Th1 or Tc1 lymphocytes. The animal model of contact sensitivity (CS) is commonly used to study ACD in mice and helps to test new therapeutics. We have previously shown that epicutaneous (EC) immunization with TNP-Ig prior to hapten sensitization inhibits Th1-mediated CS and observed that the suppression is mediated by TCRαβ(+) CD4(+) CD8(+) cells and is TGF-β dependent. More recently we have shown that EC immunization with DNP-BSA induces TCRαβ(+) CD4(+) CD25(+) FoxP3(+) T regulatory (Treg) cells that suppress Tc1-mediated CS.
Methods: Animal model of contact sensitivity was used to study skin-induced suppression.
Results: Current work employing Tc1-mediated CS shows that skin-induced suppression is dose-dependent and declines with time. Experiments with the four non-cross-reacting antigens 2,4-dinitrophenylated bovine serum albumin (DNP-BSA), ovalbumin (OVA), myelin basic protein (MBP) and immunoglobulins conjugated with oxazolone (OX-Ig) employing models of active suppression, "transfer in" and "transfer out" protocols showed that EC immunization with any tested protein antigen inhibits CS response suggesting lack of antigen-specificity of the investigated phenomenon.
Conclusion: The ease of EC generation of antigen-non-specific regulatory cells may have important implications for designing therapeutic schemes aimed at modulating immune responses.