Journal
EXPERIMENTAL DERMATOLOGY
Volume 21, Issue 12, Pages 961-964Publisher
WILEY-BLACKWELL
DOI: 10.1111/exd.12037
Keywords
AIM2; atopic dermatitis; barrier disruption; contact dermatitis; epidermis; immunohistochemistry; inflammation; psoriasis; wound healing
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Funding
- AGIKO stipend from the Netherlands Organization for Health Research and Development
- VIDI grant from the Netherlands Organization for Health Research and Development
- Dutch Ministry of Economic Affairs [PID082025]
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Absent in melanoma 2 (AIM2) is a double-stranded DNA receptor, and its activation initiates an interleukin-1 beta processing inflammasome. AIM2 is implicated in host defense against several pathogens, but could hypothetically also contribute to autoinflammatory or autoimmune diseases, such as is the case for NLRP3. Using thoroughly characterised antibodies, we analysed AIM2 expression in human tissues and primary cells. A strong epidermal upregulation of AIM2 protein expression was observed in several acute and chronic inflammatory skin disorders, such as psoriasis, atopic dermatitis, venous ulcera, contact dermatitis, and experimental wounds. We also found AIM2 induction by interferon-gamma in submerged and three-dimensional in vitro models of human epidermis. Our data highlight the dynamics of epidermal AIM2 expression, showing Langerhans cell and melanocyte-restricted expression in normal epidermis but a pronounced induction in subpopulations of epidermal keratinocytes under inflammatory conditions.
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