4.6 Article

Strong induction of AIM2 expression in human epidermis in acute and chronic inflammatory skin conditions

Journal

EXPERIMENTAL DERMATOLOGY
Volume 21, Issue 12, Pages 961-964

Publisher

WILEY-BLACKWELL
DOI: 10.1111/exd.12037

Keywords

AIM2; atopic dermatitis; barrier disruption; contact dermatitis; epidermis; immunohistochemistry; inflammation; psoriasis; wound healing

Categories

Funding

  1. AGIKO stipend from the Netherlands Organization for Health Research and Development
  2. VIDI grant from the Netherlands Organization for Health Research and Development
  3. Dutch Ministry of Economic Affairs [PID082025]

Ask authors/readers for more resources

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.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.6
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available