Abstract
Exposure to certain chemicals disturbs skin homeostasis. In particular, protein-reactive chemical contact sensitizers trigger an inflammatory immune response resulting in eczema and allergic contact dermatitis. Chemical sensitizers activate innate immune cells which orchestrate the skin immune response. This involves oxidative and inflammatory pathways. In parallel, the Nrf2/Keap1 pathway, a major ubiquitous regulator of cellular oxidative and electrophilic stress is activated in the different skin innate immune cells including epidermal Langerhans cells and dermal dendritic cells, but also in keratinocytes. In this context, Nrf2 shows a strong protective capacity through the downregulation of both the oxidative stress and inflammatory pathways. In this review we highlight the important role of Nrf2 in the control of the innate immune response of the skin to chemical sensitizers.
Highlights
Reviewed by: Caroline Jefferies, Cedars-Sinai Medical Center, United States Marie Louise Anna Schuttelaar, University Medical Center Groningen, Netherlands
In 1978, Streilein proposed that the skin has its own integrated immune function and introduced the term of skin-associated lymphoid tissues, “SALT.” He suggested that this specialized function is mediated by keratinocytes, Langerhans cells (LC) and immune-competent lymphocytes working in concert to ensure an efficient protection [1, 2]
Keratinocytes, and fibroblasts contribute to the immune response e.g., by chemokine release which leads to a rapid recruitment of circulating immune cells, mainly neutrophils and pro-inflammatory monocytes [3]
Summary
The skin was considered as a passive physical barrier protecting the internal organs from environmental assaults. In 1978, Streilein proposed that the skin has its own integrated immune function and introduced the term of skin-associated lymphoid tissues, “SALT.” He suggested that this specialized function is mediated by keratinocytes, Langerhans cells (LC) and immune-competent lymphocytes working in concert to ensure an efficient protection [1, 2]. The main resident innate immune cells in the skin, such as LC in the epidermis or dendritic cell (DC) subpopulations, mast cells and macrophages in the dermis, supervise the most exposed organ, react rapidly to danger signals resulting from biological or chemical hazards and orchestrate the immune response. Keratinocytes, and fibroblasts contribute to the immune response e.g., by chemokine release which leads to a rapid recruitment of circulating immune cells, mainly neutrophils and pro-inflammatory monocytes [3]
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