Local elevation of CCL22: A new trend in immunotherapy (skin model)

Abstract

Many evidences supported the suggestion that one of the reasons for the failure of immunosuppressant like Corticosteroides, Calcinurine inhibitors and VitD3 in reestablishing skin immune tolerance is relying on inhibition of CCL22 expression from skin dendritic cells. Inhibition of CCL22 decreases CD4+ CD25+ FoxP3+ regulatory T cells homing to macular area and reduces the suppression capacity of these cells that make a sort of an imbalance between effector and regulatory T cells. Addition of CCL22 into the skin lesion from external sources could change the ratio between effector and regulatory T cells which dramatically alter immune system and reestablish immune tolerance. This action can't be established by the later immunosuppressant (e.g. corticosteroids and calcinurine inhibitors) alone which give CCL22 an important role in the treatment of skin autoimmune and graft rejection diseases.