Psoriasis is a chronic inflammatory disease with a strong genetic component that can be triggered by environmental factors. Disease pathogenesis is mainly driven by type 1 and type 17 cytokine-producing cells which, in healthy individuals, are modulated by regulatory T cells (Tregs). Tregs play a fundamental role in immune homeostasis and contribute to the prevention of autoimmune disease by suppressing immune responses. In psoriasis, Tregs are impaired in their suppressive function leading to an altered T-helper 17/Treg balance. Although Treg dysfunction in patients with psoriasis is associated with disease exacerbation, it is unknown how they are functionally regulated. In this review, we discuss recent insights into Tregs in the setting of psoriasis with an emphasis on the effect of current treatments on Tregs and how already available therapeutics that modulate Treg frequency or functionality could be exploited for treatment of psoriasis.
The British journal of dermatology
14 - 24
Medical Research Council Human Immunology Unit, Radcliffe Department of Medicine, Oxford National Institute for Health Research Biomedical Research Centre, Medical Research Council Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
Humans, Psoriasis, Autoimmune Diseases, Disease Progression, Cytokines, T-Lymphocytes, Regulatory