Immune regulatory mechanisms in allergic contact dermatitis and contact sensitization.

Contact allergy is a very common disease due to an uncontrolled immune response to chemically reactive small molecular compounds penetrating the skin. The reaction is mostly sustained by specific CD8+and CD4+type 1 T lymphocytes, which are recruited at the site of chemical challenge thanks to the expression of specific homing and chemokine receptors. Evidence exists that specialized subsets of T lymphocytes with regulatory function modulate immune responses to haptens by preventing the occurrence of the hypersensitivity reactions in non-allergic individuals exposed to the sensitizer. In addition, the magnitude of the inflammatory reaction in allergic individuals is also tightly regulated not only by the exhaustion/ apoptosis of effector T cells at the site of chemical challenge, but also by the intervention of T-regulatory cells. Most of the T-regulatory cells involved in this process belong to the CD4+ subset, such as the IL-10-producing T cells, namely Tregulatory cells 1, and the CD4+CD25+T-regulatory lymphocytes. In addition, reports suggest the existence of Treg activity among the CD8+ subpopulation. The currently held view is that contact allergies are the consequences of the exaggerated expansion of specific CD8+ effector T lymphocytes due to an impaired development of efficient regulatory T cells.