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Strong induction of AIM 2 expression in human epidermis in acute and chronic inflammatory skin conditions
Author(s) -
de Koning Heleen D.,
Bergboer Judith G.M.,
van den Bogaard Ellen H.,
van VlijmenWillems Ivonne M.J.J.,
RodijkOlthuis Diana,
Simon Anna,
Zeeuwen Patrick L.J.M.,
Schalkwijk Joost
Publication year - 2012
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12037
Subject(s) - aim2 , epidermis (zoology) , inflammasome , immunology , psoriasis , human skin , atopic dermatitis , downregulation and upregulation , biology , inflammation , medicine , genetics , anatomy , gene
Absent in melanoma 2 ( AIM 2) is a double‐stranded DNA receptor, and its activation initiates an interleukin‐1 beta processing inflammasome. AIM 2 is implicated in host defense against several pathogens, but could hypothetically also contribute to autoinflammatory or autoimmune diseases, such as is the case for NLRP 3. Using thoroughly characterised antibodies, we analysed AIM 2 expression in human tissues and primary cells. A strong epidermal upregulation of AIM 2 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 AIM 2 induction by interferon‐gamma in submerged and three‐dimensional in vitro models of human epidermis. Our data highlight the dynamics of epidermal AIM 2 expression, showing Langerhans cell and melanocyte‐restricted expression in normal epidermis but a pronounced induction in subpopulations of epidermal keratinocytes under inflammatory conditions.