Insulin-like growth factor-1 induces regulatory T cell-mediated suppression of allergic contact dermatitis in mice |
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| Authors: | Bjarki Johannesson Susanne Sattler Ekaterina Semenova Saveria Pastore Teresa M. Kennedy-Lydon Robert D. Sampson Michael D. Schneider Nadia Rosenthal Daniel Bilbao |
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| Affiliation: | 1.Mouse Biology Unit, European Molecular Biology Laboratory (EMBL), Monterotondo, 00015, Italy.;2.National Heart and Lung Institute, Imperial College, London W12 0NN, UK.;5.Laboratory of Experimental Immunology, Istituto Dermopatico Immacolata, IRCCS, Rome 00167, Italy.;6.Australian Regenerative Medicine Institute, Monash University, Clayton, VIC 3800 Australia. |
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| Abstract: | Allergic contact dermatitis (ACD) is triggered by an aberrant hyperinflammatory immune response to innocuous chemical compounds and ranks as the world’s most prevalent occupational skin condition. Although a variety of immune effector cells are activated during ACD, regulatory T (Treg) cells are crucial in controlling the resulting inflammation. Insulin-like growth factor-1 (IGF-1) regulates cell proliferation and differentiation and accelerates wound healing and regeneration in several organs including the skin. Recently IGF-1 has also been implicated in protection from autoimmune inflammation by expansion of Treg cells. Here, we demonstrate that ectopic expression of IGF-1 in mouse skin suppresses ACD in a Treg cell-specific manner, increasing the number of Foxp3+ Treg cells in the affected area and stimulating lymphocyte production of the anti-inflammatory cytokine interleukin 10. Similar therapeutic effects can be achieved with systemic or topical delivery of IGF-1, implicating this growth factor as a promising new therapeutic option for the treatment of ACD.KEY WORDS: Insulin-like growth factor-1, Atopic dermatitis, Contact hypersensitivity, Regulatory T cells, Treg |
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