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.
Highlights
Allergic contact dermatitis (ACD) is a common inflammatory skin condition induced by exposure to frequently encountered environmental agents including metals, cosmetics, drugs and plant material
The severity of contact hypersensitivity (CHS) symptoms in mice lacking the insulin-like growth factor-1 (IGF-1) receptor on regulatory T cells did not improve after IGF-1 treatment
To study the effect of locally produced IGF-1 on tissue immune responses, we used the model of acute contact hypersensitivity in transgenic mice that express an IGF-1 propeptide (IGF-1Ea) ectopically in the skin (K14/IGF-1Ea mice) (Semenova et al, 2008), which improves wound healing and accelerates hair follicle formation and cycling
Summary
Allergic contact dermatitis (ACD) is a common inflammatory skin condition induced by exposure to frequently encountered environmental agents including metals, cosmetics, drugs and plant material. Haptens penetrate the skin and induce an innate immune response that leads to the priming of hapten-specific T cells, causing sensitization so that any subsequent exposure to the initial hapten elicits a vigorous secondary immune response at the point of contact. In humans, this culminates in the cutaneous inflammatory reaction defined clinically as ACD (Kimber et al, 2002; Kaplan et al, 2012; Vocanson et al, 2009)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
